Hi everybody, my name is Nico Lazovic and I'm a nurse anesthesiologist over at the City of Hope Medical Center in Duarte, California. I'm also a clinical instructor of anesthesiology over at the USC program of nurse anesthesia. I'm going to be talking to you about the anatomy and physiology of anesthesia. A lot of this might be review for some of you, for some of you maybe stuff that you've never heard about before, things that you've never seen, and for many of you some of this may be an expansion on some of the knowledge that you already have and stuff that you've seen in your ICUs and nursing school. So just a little bit about myself here, I was born and raised in Los Angeles, was born here, never left, did all of my training out here, did undergrad at UCLA, so I am a Bruin but I'm also a Trojan as well. I did nursing school as well at the UCLA School of Nursing because I did my undergrad in a topic that wasn't nursing. I then spent three years in a pediatric ICU which was a combined medical and surgical ICU, so we saw everything from sick airways to severe pulmonary disease, we had a large oncologic population, so we had a very, very wide breadth of patients. After that I did my nursing anesthesiology training at USC where I'm also still a clinical instructor. My first job out of school was at the Keck Medical Center of USC right across the street from the training program, and after that I transitioned to the City of Hope Medical Center where I'm proud to say I was the first CRNA there, and I have also done about three years in private practice just as a little bit of side work, doing a lot of plastic surgery, ENT, pain management, that sort of thing, and like I said I've also been a clinical instructor of nurse anesthesiology at USC for about five years, and I love to teach. If any of you end up going to USC you will see a lot of me, I run a lot of labs and I do a lot of talks on pharmacology. So some basic disclosures here, I don't have anything to disclose, I do not earn a profit from any of this, nothing that I say today could be construed as a conflict of interest, and I am not funded for any of this. Some of the course objectives today, we're going to be talking a lot about just basic anatomy, basic gross anatomy, of a lot of the structures that are most relevant to anesthesia. So you could talk for hours and hours and hours about the parts of the body that are relevant to anesthesia, but the things that I think are most relevant are cardiac, respiratory, and airway systems. We could have also talked extensively about the spine and brain as well, but I kind of wanted to get a little bit more of a focus on the cardiac, respiratory, and airway systems because I personally think they're the most interesting and the most relevant to our practice. I'm also going to be talking about a lot of the cellular and tissue physiology that relate to these systems. And then for each section I'm going to be doing a little bit of clinical application. So when you were in nursing school or maybe you had some other sort of training, you may have been learning certain anatomy and physiology and said, why does this matter? Why do I actually have to know about some of this stuff? It turns out in anesthesia, a lot of what we learn you really need to know every day. You may have wondered, why do I need to learn about the epiglottis? You will need to know about the epiglottis very, very well in anesthesia practice as when you intubate, you will see it every single time. So my goal is to make it as clinically relevant while also going into as much academic and scientific rigor as possible. We're going to start today's discussion talking about cardiovascular anatomy and physiology. A lot of this you probably already know. I'm sure you're familiar with the basic structure of the heart, the atria, the ventricles, probably basic coronary anatomy, probably basic electrophysiologic anatomy such as the SA node, AB node, etc. So I'm not going to go over a lot of that basic stuff. I'm really going to try to focus on things that perhaps you've never seen before or perhaps didn't know as much detail about. This slide is deceivingly simple. So in this slide, I'm discussing how does your body generate blood pressure? As we know, blood pressure is critical for end-organ tissue perfusion. So any organ in the body, your brain, your heart itself, kidneys, muscles, everything needs to have oxygen delivery to it, and of course that's what the heart does. Blood pressure is dependent on two main things. Cardiac output, so how much blood is the heart putting out, and we typically measure that in liters per minute, so how much is flowing out of the heart. Blood pressure is also dependent on systemic vascular resistance. A lot of times we refer to this as the squeeze of the vessels, so how vasodilated versus how vasoconstricted you are, and so that really what generates, that's really what generates blood pressure. You can almost think of it like a garden hose, right? You turn on the hose, that's how much water is flowing out of it, but then if you had a bigger hose or smaller hose, that would also change the pressure in that line, right? Cardiac output is also dependent on two things, heart rate and stroke volume, and that's just a basic calculation. So if cardiac output is measured in liters per minute, we need to know how much is coming out with each beat, so that's the stroke volume, and we need to know how often is it beating, heart rate. Seems pretty simple, but we're going to dive into a little bit more detail here. As I mentioned before, cardiac output is dependent on two things, both heart rate and stroke volume. When we think about heart rate, there's several things that influence that. The most obvious thing that we often think about is the intrinsic conduction of the heart. These include any of the electrophysiologic structures of the heart, the things that we typically think of are the sinoatrial node, the SA node, which is where conduction begins, then transfers down to the AV node, or atrioventricular node, then transfers down to the bundle of his, or intraventricular bundle, which sits between the ventricles and conducts down to the Burkinji fibers, which causes depolarization of the ventricles and ultimately results in contraction of those ventricles. The contraction of course happens in the atria as well, but we often just kind of think of the ventricles as doing a lot of the heavy lifting in terms of the cardiac output. But that's not the only thing that dictates heart rate. Heart rate is also dependent on central nervous system and peripheral nervous system influence. So things that we think of would be sympathetic nervous system influence, or SNS as you see on the slide. Examples of that would be cardioaccelerator fibers, which are released from the thoracic nerves out of the spine, and those are responsible for increasing heart rate. Parasympathetic nervous system innervation is a huge driver of heart rate as well. So the vagus nerve, which is one of the cranial nerves of the brain, innervates that SA node, which as we mentioned is that first node in the heart that dictates rate. That releases acetylcholine onto the sinoatrial node. So that parasympathetic innervation and that acetylcholine is responsible for slowing the heart. So this is a reason why, for example, if you ask a patient to bear down or perform a vagal maneuver, vagus, vagal maneuver, it releases acetylcholine onto that sinoatrial node and can slow the heart. This is another reason why, for example, cholinergic drugs such as neostigmine can slow the heart, or why anti-cholinergic drugs such as atropine or glycopyrrolate will speed up the heart. Also mentioned the baroreceptor reflex, without getting into too much detail, and you will learn plenty of detail on the baroreceptor reflex, you have to remember you have baroreceptors in your carotid bodies and the aortic arch. These respond to changes in blood pressure. As blood pressure goes down, your body detects that and then will speed up your heart in order to increase cardiac output. The converse is also true. So if you've ever given something like a pure alpha agonist to your patient, such as phenylephrine or even vasopressin, you sometimes will see a drop in the heart rate because you've increased the pressure. Of course, there's also external factors that increase heart rate. These would be things like temperature, so febrile patients can be tachycardic, stress and pain. This should be fairly intuitive. During surgery, for example, if a patient's not anesthetized enough or doesn't have enough opioid on board or other analgesia on board, a lot of times you can see a tachycardic response to surgical stimulus. And then other hormonal factors, perhaps the patient has an increase in circulating catecholamines for whatever reason. Let's say they have a theochromocytoma or some sort of other endocrine issue that leads to an increase in heart rate or a decrease in heart rate for that matter. In terms of stroke volume, there's a few things that really dictate how much is coming out of the heart with each beat. And probably the most obvious thing that we would think about would be circulating blood volume. So a patient would be hypotensive if, say, they were severely dehydrated or they were hemorrhaging. So I'm sure all my trauma ICU nurses have seen this. Or anyone who's had a patient who comes back from the OR and there's a bleed somewhere. So that would be a reason. Their stroke volume has just dropped off because they don't have enough circulating blood volume. One thing that we're going to dive into in a little bit more detail in the next slide is the linked tension relationship, also known as the Frank-Starling Law. Maybe you heard a little bit about this in nursing school. Maybe you know a little bit about this if you've taken CCR, but we're going to talk about this. Basically, the general idea here is that if you feel the heart, if you stretch a ventricle, if you stretch an atria, anything, that tension alone that you've built by stretching it causes an increased force, just like a rubber band. We're going to go into a little bit more detail in a second. Other things that influence stroke volume would be cardiac performance. So what is the patient's ejection fraction? How much can their cells actually contract with each beat? This can be dependent on various disease states. Let's say ischemic cardiomyopathy. They could have a variety of things that decrease their cardiac performance. Electrolyte imbalances are a really common one as well. Hypocalcemia, hypomagnesemia, and lastly, valvular adequacy. I'm sure all of my cardiac ICU nurses out there have seen mitral stenosis, mitral regurge, aortic stenosis, aortic regurge. I'm sure my pediatric cardiac ICU people have seen plenty of pulmonary valve pathology, and all of those can decrease stroke volume and therefore cardiac output because the blood just can't get where it needs to go, i.e. out of the aorta into the tissues. As promised, let's discuss a little bit more about that Frank-Starling law of the heart, also known as the length-tension relationship or also known as the force-velocity relationship of the heart. If we look at this graph, you can see the x-axis is end-diastolic volume. This can be measured by a variety of different metrics. It says here right atrial pressure, but it could be right atrial pressure. It could be pulmonary artery occlusion pressure, which is a proxy for left atrial pressure. Really what this means is preload. How much volume are we getting into the heart to allow it to eject? We're thinking about how much are we stretching that chamber, whether it's an atria or ventricle. I usually just kind of think of it as ventricle in my head. That kind of helps me think of it a little easier, but it could really be any chamber of the heart. The y-axis is cardiac output, and this really could be just any sort of, this could be stroke volume as well. You can see how much is coming out of any chamber with each beat. If you look at the red line, the red line is cardiac output. If you look at the middle one, that's the solid line, this would just be like a normal state. The relationship that I want you to take away from here is as end-diastolic volume decreases, i.e. as preload increases, as volume increases, you have a corresponding increase in stroke volume or cardiac output. If you look above and below that middle line, let's look at the above one. The above one would be an example of a state where there's increased inotropy, right? So this would be a situation, let's say the patient was exercising, so they had increased circulating catecholamines. Let's say that you put your patient on an Epidrip. Let's say that you put your patient on any beta-1 agonist that increases contractility. That's what that would look like. You would have an increased cardiac output for any given end-diastolic volume. The converse is also true. If you look at that dotted line below the solid line, that one shows a state where there's decreased inotropy. So a perfect example of that would be a patient with cardiomyopathy or perhaps somebody who is having NMI and so they don't have sufficient oxygen to actually contract that ventricle. One thing I want to point out with the Frank Starling Law is that this is a completely passive process. This doesn't have anything to do with the contraction of cardiac myocytes. So this is not an oxygen-dependent process. It's really, it's purely just based on the recoil of the heart. It's just like a rubber band, right? If you took a rubber band and you pulled it just a little bit and released it, it would barely move. It wouldn't snap your fingers. But if you pulled a rubber band really, really, really, really far and you let go of one side, you're going to hurt your other hand because there's so much force that came down to hit your hand. Your heart works the same way. And there are disease states and disease processes that affect this. Good examples of that would be dilated cardiomyopathy where the heart has just lost a lot of that passive contractility and it just doesn't have that same kick that a typical healthy heart has. And this is something that we, as nurse anesthesiologists, have to keep in mind in certain disease states and how this is going to affect our stroke volume and therefore cardiac output and therefore our blood pressure and therefore end-tissue perfusion to our patient. So one thing that is not shown on that previous slide is that if you continue to move right on that end-diastolic volume, as you move right on the x-axis, eventually cardiac output would actually start to drop off because you've overloaded the heart. So I'm sure most of us have seen a clinical situation where a patient is volume overloaded and there's a variety of consequences to that. Things such as pulmonary edema, cerebral edema, airway edema, just a host of problems. And so a huge part of what we do every day in the operating room is making sure that we are giving our patient the correct amount of volume. We want to put our patient on the best part of the Frank Starling curve. We want to give them just enough volume so that they have optimal cardiac performance but not so much that their cardiac output starts to drop off or that we fluid overload them. And so these days in anesthesia we've moved a lot towards what we call goal-directed volume administration or goal-directed fluid therapy. And so rather than saying we're just going to give this patient, oh I don't know, we just give them a liter of volume or two liters of volume or some calculated value, we actually base a lot of our fluid administration off of various clinical endpoints. And so these are things like blood pressure, obviously, urine output, typically shooting for 0.5 to 1 milliliter per kilo per hour, hemoglobin and hematocrit. We don't want to hemodilute our patients unnecessarily. Or the opposite, hemoconcentrate them, but that's a less common situation. We base it off of pulse pressure variation as well. So this is a more, this is a newer metric that we've been looking at that helps guide our fluid therapy. And this basically looks at how the difference between systolic and diastolic blood pressure is changing with respirations. And this is a calculated value and it just kind of helps inform our fluid management a little bit more. One thing I'll mention about fluid management as well is it's as much art as it is science. There's a lot of metrics that we look at, like the ones that I've just pointed out to you, but a lot of it is intuition, knowing how much fluid they're losing because of surgery, so we call those insensible losses. There's a variety of things that change our fluid management. And ultimately at the end of the day, one of the theoretical concepts that we like to do is put them on the right part of the Frank-Starling curve, give their heart enough preload to have good cardiac output without overloading them using some of these metrics that you can see. So another clinical application I like to talk to you guys about is how spinal anesthesia affects blood pressure. Spinal anesthesia is another type of anesthetic that we use all the time for a variety of procedures. And this would be anything typically below the level of the xiphoid process, which is like the lower part of the lung. So the most common example of spinal anesthesia would be pregnant women, parturians, right? So these are patients who we do not want to induce general anesthesia for. There's a huge benefit in doing spinal anesthesia for them, but there are a handful of risks. So spinal anesthesia involves putting a small amount of local anesthetic into the subarachnoid space. Basically this is where your cerebrospinal fluid is. So it's a very small needle, usually 25 gauge or smaller. When we inject that local anesthesia, what it causes is a decrease in nerve function of the nerves that are coming out of the spine. And this is used just as the sole surgical anesthetic for either abdominal surgery, knee surgery, things like that. And patients can be completely awake. So for mom, there's a huge benefit. Mom can be awake, she can immediately see her baby, and she has no idea what's going on during surgery, or usually only feels maybe mild pressure. The main risk that we think about, or one of the main risks that we think about with spinal anesthesia is a decrease in blood pressure. Why is that the case? That's the case because of two things, and if we think back to our original example of how do we create blood pressure, right? Blood pressure is SVR times cardiac output. Spinal anesthesia decreases both. So it decreases SVR via systemic vasodilation. When you numb all of those nerves, when you decrease that nervous transmission to the peripheral vascular system, that massive vasodilation just drops blood pressure. In addition, in the thoracic spine, there's quite a bit of cardioaccelerator fibers, as I mentioned before. Those cardioaccelerator fibers are responsible for increasing heart rate. If you numb those, your heart can no longer increase heart rate as it typically would. This leads to a bradycardia, which leads to decreased cardiac output, which leads to hypotension. So you have a variety of ways that spinal anesthesia can decrease blood pressure, but if you know how blood pressure is generated, you can know how to treat it more easily. So the vital signs that you see here, heart rate of 46, blood pressure of 71 on 35, this should not be an uncommon blood pressure, er, hemodynamic profile to see in somebody who you were doing spinal anesthesia on. So how would you intervene with this patient, okay? Would you give them a vasoconstrictor? Well, maybe, but you might decrease their heart rate even worse. Would you give them something that's just going to increase their heart rate? Maybe, that might help, but then you still have to drop an SVR. So we're constantly thinking about these things. What is the ultimate problem going on with this patient? What medications do we need to give to treat them? I'll mention also that a lot of the drugs that we give, they're based on these anatomical and physiologic principles. You have to understand these really well before you can know how to treat them. Next up we're going to move to respiratory and neuromuscular anatomy and physiology. You may wonder why I grouped together neuromuscular anatomy and physiology into this group. That's because neuromuscular blockade and neuromuscular physiology plays a particularly large role with the respiratory system, especially with the drugs that we use in anesthesia. What you're looking at here is a basic spirometry curve, and what we're going to assess are the different capacities and different volumes that are present in the lungs and how they're affected by anesthesia. So what you're looking at on the x-axis would just be time. So basically you're looking at somebody taking a breath. The y-axis is the amount of volume. So for example, if you look on the blue curve, this is the spirometry, we're moving up and down. So as we move up, that's inspiration. As we move down, that's expiration. Now if you continue to move to the right, you'll see the patient takes a big inspiration all the way up, and then they do a big exhalation and they forcefully exhale all that volume and they come back to normal breathing. So some of the things that I'd like to point out here is normal breathing is on the left. So that would just be a normal tidal volume, just in and out. Tidal volume is how much we take in and out with one breath. Now everybody here who has lungs and can breathe knows that if you want to, you can take a bigger breath. That volume is referred to as inspiratory reserve volume. And so that's the maximal amount of lung air that you can get into your lungs. And so you see here labeled, that's IRV. Anybody also with lungs knows that if you want to, you can exhale more than you comfortably could. So if I'm just breathing right here, expiratory residual volume would be, I'm here normally, and I blow out the remaining amount. Now what's kind of interesting to me is that after you do that, there's actually quite a bit of air left in your lungs, and we call this residual volume, or RV, which you can see labeled here. Now you can see IRV, TV, ERV, and RV here. These are all volumes. The rest on the right are all capacities, and these are just really calculated volumes that are just kind of helpful for us to think about. One that I'll point out here is VC, or vital capacity. Vital capacity just refers to the amount of air that you can take in and out of your lungs with your volition. Like if you want to, you could breathe in as deep as you want, that's IRV, and then forcefully exhale as much as you can, no amount of breath, that would be all of your expiratory residual volume. So that whole thing would be your vital capacity. You can see that could also be broken into inspiratory capacity, that's at the end of a normal exhalation, how much you can maximally breathe in. And then the last one, now this one is pretty interesting and pretty important to anesthesia practice, FRC, functional residual capacity. So this is a calculated value of residual volume, so that's how much is left in your lungs after a maximal exhalation, and your expiratory reserve volume. On the right you'll see TLC, total lung capacity, that's just, you've got to go with what it sounds like, the amount of air that can totally fit in your lungs. To go back a second to FRC, functional residual capacity, why does this random value deserve so much attention in anesthesia? Basically FRC, you can think of it as a measure of your intrinsic PEEP. It's the amount of air that's left in your lungs after a normal exhalation, so it's amount of air that's keeping your lungs open. This air is responsible for keeping the alveoli open, this stops alveolar collapse, it helps to keep your SATA. Why do we care in anesthesia? The reason that we care is because anesthetics and paralytics profoundly reduce FRC, profoundly, on the induction of anesthesia. So virtually all patients who we induce general anesthesia on have an immediate drop in FRC, and we need to do, we need to have interventions to make sure that they don't inappropriately drop their SpO2 and PaO2, okay. You can think of this as, let's say that you had a critical care patient and they're on a PEEP of 14 and you're working to keep their SPO2 up, imagine you just took the knob and just turn the PEEP to zero. That's what we do with anesthesia in healthy patients. We drop their PEEP to zero functionally by destroying their FRC. The reason this happens is because FRC is largely maintained by passive neuromuscular function. So a lot of this is your diaphragm has an existing resting muscular state, intercostal muscles, and a lot of other muscles of the supporting cast. When you give paralytic, when you give anesthetics that make a patient apneic, you lose all of that tone and therefore your lungs recoil in and you lose FRC. A lot of what we do from the respiratory perspective for our patients interoperatively focuses around optimizing FRC to assure that our patients don't get an adelectatic and to maintain their SpO2. Let's also talk about VQ matching in lung zones. So what VQ matching is, is it refers to the relationship of how well ventilated an area of the lung is and how much blood that area receives. So in VQ, V refers to ventilation, Q refers to perfusion. Don't ask me where the Q comes from. It's probably because they just didn't want to use P and confuse people. So a typical ratio of V to Q is usually around 0.8, right? So the normal ventilation is about 4 liters per minute, perfusion is about 5 liters per minute to the lung. So it's usually around 0.8 in that ballpark, okay? So it turns out that there are differential VQ areas in the lung. We refer to these as lung zones and they're named after someone named West, so we call them West's lung zones. Zone one is the top and so it is the top of the lung, the apex of the lung. So we would call, in that situation, the alveolar pressure of the lung, i.e. the ventilation, is much higher than the blood flow to that area. And so you would end up with a VQ ratio greater than one. In the middle, zone two, arterial pressure and alveolar pressure are pretty close to the same. Arterial pressure is marginally higher, so we see the VQ ratio is around one there. And then in the lung base, just because of gravity, there's more blood flow at the base of the lung but there's not as much perfusion. And so you end up with a situation where VQ is under one. Why does this matter? This matters because these West lung zones, these exist with us just standing in a normal position. Do we do surgery standing? Shake your head and say no. We do it with patients laying supine. We do it with patients on their side. We do it with patients with their legs up, with their heads down, with their heads up. All sorts of different positions. So we have to think about how are these West lung zones changing? How is my VQ matching changing depending on a patient's position during surgery? One thing I'll mention as well is hypoxic pulmonary vasoconstriction. I think this is a very fascinating and very clinically relevant topic. Basically your body is very smart. Let's say that you had an area of the lung that's normal, right? So you have a certain amount of ventilation in that lung area and you have a certain amount of perfusion that's going over it. Now let's say, for whatever reason, let's say that air stopped flowing into that region and blood continued to flow over it. Is that blood gonna get oxygenated? No. So then you have deoxygenated blood that's gonna ultimately return back to the heart. How does that present clinically? Decreased SpO2, right? But the body's very smart and the body says, hey, via a variety of intracellular mechanisms that you will learn the details of in school, through a variety of mechanisms, your body says, hey, there's no ventilation in this area, there's no oxygen in this area, stop sending blood here because it's gonna go back to the heart deoxygenated. And so it vasoconstricts that whole area, shunting the blood to other areas of the lungs. We call this hypoxic pulmonary vasoconstriction and this is, this is adaptive. Anesthesia, most anesthetics, not all, but most anesthetics blunt hypoxic pulmonary vasoconstriction, leading to desaturation. This should matter to us for pretty intuitive reasons. Once you start giving a patient anesthesia, you're blunting HPV and decreasing their SAT. That, with the addition to you're making them apneic with our anesthetics, and also, as I mentioned before, you're decreasing their FRC, patients under anesthesia are at a huge increase of, a huge increased risk of hypoxemia. I'm gonna do a bit of a transition here and talk a little bit about neuromuscular transmission. You will learn about this extensively in anesthesiology school. So what you're looking at here is the neuromuscular junction. So this is basically the connection between the peripheral nervous system, which ultimately attaches to the central nervous system, and the muscle. So this is what's responsible for functional muscle control as well as your diaphragm. What happens is an action potential runs down some nerve fiber and when that happens it causes an increase in intracellular calcium. When that intracellular calcium is released, it causes these vesicles, these are these kind of little bubbles in the top part holding acetylcholine, or ACH, it causes them to fuse onto the cell membrane. What this does is it forces acetylcholine into that synaptic cleft, which is the gap basically between the neuromuscular junction, and that acetylcholine is then able to bind to acetylcholine receptors on the motor end plate, which is the bottom part of the screen. But it turns out that neuromuscular transmission is not just that simple. There's a few more details that matter quite a bit. So it ultimately turns out that it doesn't require one acetylcholine molecule to bind to the acetylcholine receptor to cause movement. It actually requires two acetylcholine molecules. This will become relevant later. It turns out it's not just any acetylcholine receptor, but these are specific types of acetylcholine receptors, nicotinic acetylcholine receptors, which are present on the motor end plate. This is different than the muscarinic acetylcholine receptors that are found in other places in the body, and you will go into extensive discussion during class about these. When you have two acetylcholine receptors that bind to a nicotinic acetylcholine receptor, it causes a few things in the cell. It causes sodium and calcium influx, and it causes potassium efflux. Influx is into the cell, efflux is out of the cell. Ultimately what ends up happening, though, is because of this nicotinic acetylcholine receptor agonism, you end up with postsynaptic decolorization, or an action potential that forms, which leads to excitation-contraction coupling. What that means is how the electricity causes some force change, and you will learn extensively about that as well, and then ultimately force is created, and this is how muscles work. But if you thought it ended there, you would still be wrong. There's still more details about this process that are relevant to us. So acetylcholine receptors, like I said, there's two types. There's nicotinic and muscarinic, and really an acetylcholine receptor is any receptor that binds to the ligand acetylcholine. Nicotinic acetylcholine receptors are ionotropic, meaning that they allow flux or flow of electrolytes past them, and the reason they call it a nicotinic acetylcholine receptor is that it also binds...you can also use nicotine as a ligand. So it's kind of interesting. Back when they were studying this stuff, they would just kind of squirt chemicals on them and see what worked, and it turns out nicotine was one of them. Nicotine is found in nitrate plants such as tobacco. It's found in other stuff as well, but tobacco is usually the one that we think of. Kind of weird, right? These nicotinic acetylcholine receptors, like I said, are found on the motor end plate, but they're also found in a variety of other places such as the autonomic ganglia, as well as the brain. As mentioned, there's also muscarinic acetylcholine receptors. These bind to, unsurprisingly, muscarine, which is found in a variety of plants as well. And muscarinic acetylcholine receptors are found throughout the body as well. These are typically found in smooth muscle. They're often found in nodal tissue in the heart. So when we think about why certain acetylcholine antagonists or acetylcholine agonists work on certain systems and not others, it's usually because they're working on either the nicotinic or the muscarinic. So consider this. You've no doubt heard of rocuronium or sesatracurin. These are acetylcholine receptor antagonists, but then if you think of atropine, atropine is also an acetylcholine antagonist or at least works on the acetylcholine system. Why don't drugs like rocuronium and sesatracurin then cause tachycardia? Why don't they work on the SA node and block SA node function and cause tachycardia? And the reason is is because those types of drugs, the paralytics that we work with, only work on nicotinic acetylcholine receptors, whereas drugs like atropine or glycopyrrolate, which are also anticholinergics, only work on muscarinic receptors. So kind of interesting fun fact there. And if you thought it stopped there with acetylcholine, it does not. You will learn so much about acetylcholine that you never thought possible. So you're gonna learn all about the acetylcholine cycle and I'll teach you a little bit about that now. So it turns out that acetylcholine is made from a combination of choline and acetyl coenzyme A, also known as acetyl CoA. Choline is taken in from extracellular fluid through sodium-dependent active transport, so it's moved from outside the cell back inside the cell using ATP, basically using active transport. Acetyl CoA is actually a product of glucose metabolism through the Krebs cycle. You've probably heard the Krebs cycle and thought you'd never hear it again. You're gonna learn so much about the Krebs cycle and this is one of those situations where it's actually kind of relevant because one of the products of it is acetyl CoA, which is important for acetylcholine synthesis. Once you take acetyl CoA, put it next to choline via a choline-acetyltransferase, which is an enzyme, you get acetylcholine, which is responsible for all these wonderful processes that we've discussed so far. Let's talk a little bit about the metabolism of acetylcholine as well. So acetylcholine is metabolized by acetylcholinesterase or ACHE. You'll often see it as broken down, and it's broken down into choline and acetate. And remember, choline is ultimately going to be reuptake and reuse, so the body recycles that choline. Acetate is usually cleared through the urine and then, like I said, the body will create more acetyl CoA via the Krebs cycle and the cycle continues to repeat itself. You don't need to eat acetylcholine. You don't need to bring it into your body. Your body just produces this on its own. What's that I heard you say? You want to learn more about acetylcholine? Okay let's learn more about acetylcholine. This is the last slide that I give you guys on acetylcholine. This is just a visual representation of what I discussed in the previous slide. So if you look at the middle of the screen, you'll see this kind of white dotted area, and that's the synaptic cleft. That's the space between the presynapting and postsynapting neuron where acetylcholine is released. Let's move our way to the right. We'll see that acetylcholinesterase or ACHE is breaking acetylcholine down into two things. Acetic acid or acetate, as we mentioned, and choline. Choline is moved back into the cell to be reused. Acetic acid is just going to be cleared, usually recently. That choline re-enters the cell via an active process, as I mentioned, and then if you look at the top right of the purple area there, that's acetyl coenzyme A or acetyl CoA, which is created through the Krebs cycle. Acetyl CoA combines with choline via choline acetyltransferase to create acetylcholine again, and then it's put into a acetylcholine vesicle where the entire process starts again. So like I said, if you like acetylcholine, you are gonna get so much explanation of it during school, and you're gonna learn more details about it than you ever thought possible. So why does any of this stuff matter? Is this just all high in the sky, ivory tower stuff? The answer is absolutely no. This is not just stuff you learn in school, this is stuff that you see clinically all the time, and your understanding of the anatomy and physiology can really change a patient's outcome. So the clinical application of some BQ matching, hypoxic pulmonary vasoconstriction, and spirometry. So like I said, lung zones are dynamic, they change depending on the patient's positioning. So let's say that a patient had had a lobectomy before, a surgical removal of part of their lung, and then you put them on their side so that that that part of the lung is now down. Well that part of the lung, there's nothing to perfuse there. The rest of the rest of the the rest of the lung has to do extra work, basically. How is that going to affect your patient's SAT? How does patient positioning in that unique clinical situation, how is that going to affect your patient? Should you give them more PEEP? Should you request the surgeon that we work in a different position? Are there medications that we can give? As I mentioned before, hypoxic pulmonary vasoconstriction is extremely relevant to our practice because most of our anesthetics blunt HPV to a certain extent. This might manifest in decreased SpO2 or decreased PaO2. So what are some of the things that we could do to help support a patient's SAT once we've blunted HPV? Could we increase the PEEP in this patient? Could we increase the FiO2? What are the risks of increasing FiO2? Are we going to cause the patient to become more adalectatic through diffusion hypoxia, or through diffusion adalectosis, excuse me, because we've then given them more FiO2? Let's look at a little bit about spirometry as well. As I mentioned, because you're losing that neuromuscular tone, you're causing a profound decrease in functional residual capacity. So that residual volume and that expiratory reserve volume are just collapsing. So that's basically the body's intrinsic PEEP. What do we do for these patients to help optimize their SAT in the face of all these negative pulmonary sequelae? So can we do things like give PEEP? Notice a trend here. Should we increase the FiO2? Should we cause a position change? Should we not give paralytic? Should we not give as much anesthetic? How does this affect patients with with pulmonary diseases such as asthma? And this is all stuff that you guys are gonna learn in school, but you have to understand this anatomy and physiology to really understand how the pathophysiology affects it and how our treatments change. Lastly, all of our anesthetics cause respiratory depression and apnea. So if that's the case, how do we keep our patients safe interoperatively? Right. Do we always have to put in a breathing tube? Do we always have to put in an LMA? Are there situations where apnea is a good thing, where we want to control the ventilation? And these are all things that you guys are going to learn in more detail during your anesthesiology training. Let's discuss a little bit about the clinical application of learning about the neuromuscular junction. Now we use drugs that take advantage of the neuromuscular junction virtually every day in anesthesia, and these are our paralytics, or some refer to them as muscle relaxants, but I typically say paralytics. So these drugs are extremely important for our clinical practice. They allow us to intubate more easily, and they allow fascial slack to allow surgeons to do what they need to do. They exert their effects on that acetylcholine receptor, that postsynaptic nicotinic acetylcholine receptor, and they just act as peer antagonists, at least the nondepolarizers do. And I'll leave the rest of the details of that to Dr. Jerome discussing your pharmacology. These drugs profoundly affect spirometry. First of all, the patient doesn't have any respiratory effort when they're under the influence of these drugs, so automatically that profoundly changes everything. As I've mentioned before, they also cause a complete collapse in FRC, leaving our patients very, very prone to desatting very quickly. What happens if we don't reverse the effects of these drugs or antagonize the effects of these drugs? Clinical signs of badness may occur, and that, that's my joking way of saying you must antagonize these drugs before you extubate a patient. One, these patients are not able to breathe on their own, of course, and two, these patients are not able to maintain a patent airway on their own. So we'll discuss a little bit more with that when we talk about upper airway in the next section, but you will learn extensively about the consequences of inadequate neuromuscular blockade reversal, how to monitor that, the different drugs that we can give, the different antagonists that we can give, such as neostigmine, as you can see on the bottom left, as well as sigamin X, which is one of our newer drugs, one of the biggest revolutions in anesthesia in the last 20 years at least. Are there certain disease process processes that can affect the neuromuscular junction? Absolutely. There are a host of neuromuscular diseases, Duchenne's muscular dystrophy, a wide variety that we have to consider. Myasthenia gravis is a very common one that we see, and so we have to understand very well how those disease processes affect the neuromuscular junction and therefore how our drugs are affected by them as well. Let's move along to our last section here, upper airway anatomy and physiology. Now I've chosen to just focus on upper airway, and this involves anything basically above the glottis and above, so the vocal cords and above. I'm not really going to talk about the lower respiratory anatomy. We could. We could spend hours on it, but I think this is a little bit more interesting and maybe some stuff that a lot of you haven't seen in as much detail yet. So this is the respiratory tract. This is just a basic summary. As I mentioned before, the upper airway involves everything from the glottis and above or larynx and above. So that would be things like the nasal cavity, the pharynx, the mouth. All of that is considered to be upper airway. Lower airway would be things like the main stem trachea, both of the primary bronchi. All of the bronchioles are considered lower airway lungs. And it's really important to understand that concept between upper airway versus lower airway because our treatments will change depending on what's going on. And I'm sure a lot of you are familiar, particularly those who work medical ICU, it's important to know what the difference between, say, stridor, which is upper airway, versus wheezing, which is lower airway, and how those treatments change depending on the anatomy. Let's get into a little bit of the nasopharyngeal anatomy. Now I venture to guess most of you don't know this in a lot of detail, but you will absolutely learn all these details. Let's talk a bit about them. So what you're looking at is the lateral portion of the nasopharynx. So it's as if I turned like this. So you're looking at this lateral portion. So let's just start with the airflow, right? So the nasal vestibule would be where air enters. So this would basically be the nare or nostril. You know it. Air starts to flow up. And you'll see that there's what looks like, what, three passages here. These are separated by what are called turbinates. And so you have the inferior turbinate, the middle turbinate, and the superior turbinate. These turbinates are just bone covered in epithelial tissue. Both the superior and middle turbinates are part of the ethanoid bone, but the inferior turbinate is actually its own bone, which is, which is unique from that. If you remember from other anatomy classes that you've probably taken, the ethanoid bone is just one of the bones of the skull. It's that anterior bone of the skull. The function of the turbinates is to moisturize air, warm air, and filter air. And I have another slide on that, but I'll just mention it while we're here as well. So let's move a little bit past the turbinates. If you start to work down the, that kind of curve that you see, you'll see the nasopharynx. So that's basically the back wall of the pharynx just past the nose. That's like the first, like, wall that your, that air hits as you're breathing. And then it starts to flow down. Around here you can also see the eustachian tube orifice. This is basically the connection between your throat and your ear. So if you've ever yawned and you felt that equalization of pressure, you're just opening that eustachian tube and equalizing the pressure between your throat and your ear canal. Here you can't really see them very well, but there's also the adenoids as well as the tonsils a little bit lower. It's more like the oropharynx, but you can see how it's all combined. One thing I mentioned too, the coanae. These are openings between the nasal cavity and the nasopharynx. So that would kind of be right around that curve over by the eustachian tube orifice that I mentioned. Here we're looking at the sinuses and the pharynx. The sinuses don't really affect us too much. We do a good amount of surgery on them, either dilating orifices to the sinus or endoscopic sinus surgery, but these are basically just holes in the skull that allow airflow. Something that's very fascinating to me is that this is an unknown part of science. We actually don't really know why we have them. It's pretty unclear. It might be related to sound reverberation allowing us to hear a little bit better. It might be another, it might be a way to lighten the weight of the skull and to not have as much weight in your head, but ultimately, kind of unknown why we have sinuses, which I just personally think is fascinating that we haven't figured that out yet. If you look on the right side of this picture as well, you can kind of see a better orientation of where the sinuses are. You can see how that nasopharynx starts to line up with that oropharynx as well, giving us a better view of the nasopharyngeal anatomy. Moving on from nasopharyngeal anatomy, let's talk a little bit about oropharyngeal anatomy. So this is the mouth and the throat, so oro and pharynx. Some of these structures may seem obvious to you. So, for example, the lips, that's considered part of the anatomy. The tongue, very relevant, very important during laryngoscopy. And teeth. Virtually every anesthetic preoperative assessment you do, you will do an assessment of the teeth. You may have never thought that you would need to do that, but it's very relevant to us because we need to document the structure of the teeth preoperatively in case we cause any trauma to the patient during laryngoscopy or other area of manipulation. Other things to look at here. You can't really see it as well, but the hard palate would be the arch, kind of just past those top teeth, and that is comprised of the maxilla and palatine bones of the skull. You can see the soft palate just past that. That's that soft squishy part attached to the uvula, which is the dangly part in the throat. Everybody kind of wonders what that is. Function of that, also not terribly known as well. Palatine tonsils, you can see those in the back right. This cartoon patient has pretty small tonsils, almost looks like they've had a tonsil like to me, like very small, but I have very large tonsils, so perhaps they just look small to me. You can see the base of the tongue there as well, and yeah, and this is just a basic anatomy. What you're looking at here also is what we would look at during a Malampati score. So I know somebody else is talking to you about airway. You are going to do this exact review for virtually every patient. Say, open your mouth, stick your tongue out, say, ah, this is what we're looking at. This is the exact same thing as the previous slide. We're just looking at a lateral portion, so like I said, as if it was just like this, but just a cutaway. Other things that I'll point out here, you can see in pink, that's like the oral cavity in the tongue. The oral cavity is really, all the real estate in there is sucked up by the tongue, so the tongue is a big pain in the butt when we're doing airway management. You can see in purple, that is the pharynx, both the naso and oropharynx and laryngopharynx. Yeah, you can see the glottis. One thing I really want to point out to you, team, is you can see in green, that's the glottis. Okay, so that's like the glottic opening and just the upper airway. I want to point out to you that the glottis and the airway are anterior to the esophagus. Okay, I really want you to remember that they're anterior to the esophagus. So we'll get into a little bit more detail in just a second on how the epiglottis helps close the glottis during swallowing, but I want to point out in this slide just how the oropharynx, nasopharynx, and laryngopharynx are ultimately all connected and then they split off right around that level of the glottis. Here we're looking at the glottic anatomy. You will see this view thousands of times in your career if you decide to become a CRNA. You will see this all the time. Every anesthesia provider knows this very, very, very well. What you're looking at is basically the view that you would see during laryngoscopy, whether you're looking with a video laryngoscope or direct laryngoscope. Now to orient you, the top of the screen is anterior. The bottom of the screen is posterior. So what would be out of range of this picture? What would be on the posterior side? Give me a second. If you said the esophagus, you're correct. So the esophagus sits just inferior to this. Let's go through the other structures. Okay, so the big one that I want to point out here is this curve at the top of the screen. This is the epiglottis. So epi, around, glottis, glottis. So it's around the glottis. The function of the epiglottis is to cover the glottic opening as you swallow. Okay, so when you swallow, you're moving that glottis to cover the glottic opening. This prevents you from aspirating. As you could probably assume, the epiglottis is a critical structure for survival. Other big things that we're looking at here, the vocal folds, also known as the vocal cords. Now there's two of these. They're in the middle of the screen. In the middle of that is the trachea, right? So the vocal cords on each side of the trachea, these open when we're breathing and as we're talking, they vibrate and they create sound as we exhale. So right now my vocal folds are working very, very hard to talk to you guys. Just laterally on each side of the vocal folds, the vocal folds are the ventricular folds, also known as the false vocal cords. These are basically just ligaments that attach the vocal folds to the thyroid cartilage and epiglottis. They're also responsible for helping with the movement of the of the vocal folds. Other reliving structures that we think about are this area epiglottic fold. This is that lateral fold that you can see on the right. I want to point a couple little cartilages out, the cuneiform and corniculate cartilages on the bottom. These really don't affect us too much, but you see it on every laryngoscopy. A lot of people falsely call these the the aretinoids. These are not the aretinoids. The aretinoids are actually deeper and more lateral and you cannot visualize them on laryngoscopy. So I've taught you something that you could teach a CRNA or an anesthesiologist and they say, I can see the aretinoids. It's like, no, you can see the corniculate and cuneiform cartilages. It's a little fun fact for you to know. So I mentioned some of the functions of the structures that we talked about so far, but let's just kind of double-check them. So looking at the nasopharynx, the purpose of that is, you know, obviously it's a passage for air. The nasopharynx is an airway, so it allows us to breathe in and out. It's nice to breathe through the nose because it warms and moisturizes the incoming air by the turbinates. The turbinates just increase surface area that's exposed to the warm, wet, and mucous membranes, and so by the time that air gets down to our lungs, it's nice and warm and wet and filtered. The oral cavity and oropharynx does a few things. It's a passage for air, of course. It's responsible for chewing, for mastication, as well as phonation. You can't breathe through your nose, I don't think. You can't really breathe just through your nose. You've got to use your mouth, and so it's pretty important for that. The larynx is of critical importance. It's for the passage of air, of course, and it's for speaking. The epiglottis is critically important as well, which is part of that larynx, which also covers the glottis and allows us to swallow without aspirating. So if you didn't have an epiglottis, you would be in pretty big trouble and probably need a trach to protect your airway. The vocal folds can do a variety of movements. They can abduct, meaning they can open, they can adduct, they can narrow, they can tense. One of the things that we always worry with the vocal folds is laryngospasm, right? There'd be a forcible closing of the vocal cords, very scary clinical situation, and you will learn how to manage that very, very well. One thing that I want to point out here as well is if you look at the function of the nasopharynx and oropharynx, it's to warm, moisturize, filter air. If we put an endotracheal tube in, your body loses the ability to do those things, so then you're giving them very dry, very cold, often unfiltered air. So that's a lot of times why we put humidifiers on an endotracheal tube circuit that work as filters as well. So that's, if you've ever wondered why you really need those, it's because we're bypassing the function of the nose. Lastly, let's do some clinical application here. Let's talk about oral intubation. So I'm sure virtually every single one of you has seen an intubated patient almost always orally. So the goal when we place an endotracheal tube is to place a tube, an endotracheal tube, through the glottis via the mouth. And the way that we do this, I'm not gonna go into too much detail, you're gonna get an entire other airway discussion, but I'm gonna kind of emphasize the anatomical structures that we're looking at as we do this. So you're gonna open the mouth, you're gonna be very cautious of the lips. I know it seemed obvious when I say that the lips are part of the, are part of the airway, but it matters. You don't want to bust your patient's lip. Every single one of you will do it. Virtually every anesthesia provider has busted somebody's lip, not fun, but the lips are there, they're important. Teeth, we're going, usually we use a scissor technique to open the mouth via the teeth. That's why you, one of the reasons why we have to assess a patient's mouth. What if they had a loose tooth and you didn't know? They had a molar there, you push down on the molar and break it. Happens, okay? Open the mouth via the teeth, place the blade into the mouth. The classic thinking is that you're supposed to sweep the tongue out of the way. You're supposed to kind of push it to one side or the other. There's kind of a variety of perspectives on that. You slowly advance that blade along, along the tongue, and then you're gonna visualize every structure along the way. So you're looking at the tongue, you're looking at the hard palate, the soft palate, the uvula, and then you're gonna start to enter the oropharynx. Now if we're looking anteriorly, right, if we have the blade in the mouth and you're looking at the anterior side, what structure do you think you're gonna see? If you said epiglottis, you're correct. So you're gonna see the epiglottis. Now there's two primary types of blades that we use, either a curved blade or a Macintosh blade or a Mac blade, you'll see it called. That's the top photo right there. Typically advance that into the vallecula. The vallecula is that space between the epiglottis and the base of the tongue. You pull up and that allows you to see the glottis, and then you put your tube in. If you are using a Miller blade, you do not go into the vallecula. The classic thinking is to take the Miller blade, put it right on top of the epiglottis rather than in the vallecula, pull up, and you should be able to see the glottic open. Big thing I want to point out is that when you're intubating, and you will learn this, but when you're intubating, you never curve back. You're not, you're never gonna see his tongue gonna do this motion. It's always lifting. Lift up. Lift towards the corner of the room and that will really help you prevent breaking any teeth and will help you get a better view. After that you're gonna advance the endotracheal tube just past those vocal folds. You're gonna get that cuff just past, inflate the cuff, connect the circuit, start the ventilator, wait for end-tidal CO2, and you just make your patient safer. Here's an actual view of the glottis. So this is not a cartoon, this is a real glottis. So a few things to point out. You can see the epiglottis on the top side. You can't really see that how it flops down because the photo is a little kind of posterior. Obviously I can't take the photo of myself so it's kind of tricky to get a good one, but you can see the glottis is the actual opening between the vocal folds. You can see the vestibular folds, which are the false vocal cords on the side, but then you can see the true vocal cords right there. They're kind of a little bit wider than the other structures around it, but not terribly wider in this photo. The trachea. One thing I want to point out with the trachea is you can actually see the tracheal rings in this photo very well. So this is a very, very good view. Remember those tracheal rings are cartilaginous rings that help keep the structure of the trachea. Lastly you can see the corniculate and cuneiform cartilages on the bottom. Those are those kind of little ball looking things. And for this patient you would just put the tube directly in, just until the cuff is past those cords, pull your blade out, inflate the cuff, start the ventilator, wait for end-tidal CO2, and you're good to go. But we don't just do oral intubations. We do nasal intubations as well, and we do intubations beyond that. We can intubate stomas, we can do retrograde intubations, we can do double luminated tracheal tube intubations, but here's just a fun one to talk about. Nasal intubations. This is personally one of my favorite procedures to do. I love doing this procedure. I think it's a lot of fun. So, but you have to understand the anatomy very well, otherwise you could hurt a patient doing this procedure. So the goal is the same as oral tracheal intubation, right? We want to get that tube into the glottis, but how do you get the tube from the nose into the throat? How do you make sure that you end up in the trachea instead of the esophagus? You do it like this. What you do is, it requires extensive patient preparation. So first, you're usually going to use atomized oxymetazoline or some other nasal vasoconstrictor preoperatively, and this will minimize the risk of bleeding. All of these structures in the nose are highly vascular, right? Anyone who's ever had a nosebleed can tell you how profusely it bleeds. So you want something that's a vasoconstrictor in there so that when you cause a little trauma, and you will almost always cause at least a little trauma, it doesn't just bleed all over the place into the airway, which is dangerous. The other thing that most people will do is they'll ask the patient, do you have one nostril that you breathe better through than the other? And this is to assess for things like deviated septum. Like if somebody had a deviated septum all the way to one side, you're not going to try to place a tube in that side because it's occluded. So you're going to see which area they breathe through better. You're also going to want to make sure that you prepare the tube. Now the tube for nasal intubations, which I'll show you in the next slide, it needs to be very malleable because it's going along a huge curve. You need to make sure it's super, super flexible. And so one way that most people will do that is they'll take it and they'll put it in a bottle of warm saline, and that just kind of makes it really flexible and bendy. After that you're going to induce general anesthesia like you would for any intubation or for surgery. And then what most people would do is they will serially dilate the nostrils in the nasopharynx using nasopharyngeal airways, usually like a 28 through 32 French. Well lubricated, and you just go 28, take it out. 30, take it out. 32, put it out. Maybe even a 34, in and out. There's just, it's kind of an assessment because it allows you to see how patent is that nasopharynx, and it just kind of moves any soft tissue to the side in preparation for putting in your nasal tube. After this you're going to introduce the nasal ET tube into the nare with the bevel medial and slowly advance it until it is, until you can visualize it in the oropharynx. You can just open the mouth and you can just see, can I see the tube right in the oropharynx. After that you perform laryngoscopy just like you did in the previous step. So you can do direct laryngoscopy and just look directly with your eyes, or you can use a video laryngoscope. Once you have a view of the glottis, you're going to advance the tube. Now sometimes if you're lucky when you advance the tube, the tube will just go straight into the glottic opening. Easy peasy lemon squeezy. Oftentimes it doesn't, and so you have to use a special device called McGill forceps, reach into the mouth, and advance that tube into that glottic opening. After that it's the same steps, right? So cuff goes up, connect the circuit, wait for end-tidal CO2, and you're good to go. And these patients can have nasal tubes for a while. So this, these are commonly done for patients who are having extensive dental surgery, extensive oral surgery, any sort of flap reconstruction of the face, anything where the surgeon is going to be operating in or around the mouth and doesn't want a tube hanging out. And this is a discussion that you typically have with your surgeon. So just a few words of caution with the nasal intubation and some more explanation as to why you want to understand the anatomy very well. Most of the structures in the nose are highly, highly vascular, so any trauma to them can cause extensive bleeding. I've talked to numerous anesthesia providers before who have not put the bevel of the nasal tracheal tube immediately, they've placed it laterally, and what this does is it causes the pointy part to cut off a turbinate. I've had, I've had people, like I said, have cut off entire turbinates and caused extensive airway bleeding. This can be an airway emergency and can be prevented if you understand the anatomy a little bit better. It's not just the turbinates that can, that can cause trouble, you can cause trauma to the nasopharynx, to the soft palate, to anything else in there, and you really want to understand where you are with the endotracheal tube when you're performing this procedure. Some of the equipment that you're seeing in this photo on the top right, that's the nasal endotracheal tube. You'll notice that it has a preformed curve to it, which is very, very nice for us. That curve at the very top of the photo there, that's what sits at the very edge of the nare, so the tube will end up coming off like this and your circuit goes behind. The bottom right are McGill forceps, remember those are what we use to advance that tube through the oropharynx into the glottic opening, and the bottom left are just nasopharyngeal airways, which you've probably seen before and you will get extensive experience using during your anesthesia practice. So that pretty much does it for anatomy and physiology of anesthesia. This is, these are the cliff notes, these are just the things that I find personally interesting that I think are the most clinically relevant. We could have talked extensively about spinal anatomy, we could have talked more about cardiac anatomy, we could have talked about gastrointestinal, like we could just keep going on and on and on and you will get hours and hours and hours of explanation of anatomy and physiology during your CRNA training if this is the right path for you. I hope you guys gained a little bit, I hope I could facilitate a little bit of excitement in this career for you and show you some things that are gonna be a lot of fun for you in your clinical practice as a nurse anesthesiologist. I wish you all the best of luck in the future and I hope to see you around. Take care.

anesthesia

cardiovascular system

respiratory physiology

neuromuscular junction

upper airway anatomy

cardiac output

ventilation-perfusion

acetylcholine

intubation

nurse anesthetist