The autonomic nervous system is one of the most important things for you to understand because as you're providing anesthesia many times, most often the only thing that you're going to see in order to be able to determine the lightness or depth of the patient in terms of their anesthesia plane is by looking at the autonomic nervous system. So knowing the autonomic nervous system is incredibly important for you to make informed decisions as you're caring for your patient during an anesthetic. Hey future CRNA, welcome to the CSBA podcast. CSBA has helped over 3,000 nurses like you gain acceptance into schools across the country. Tune in for inspiration and actionable takeaways to help you from start to finish. Hello, future sin. Welcome back to CSBA podcast. We have a very special guest host episode for you today by Dr. Elijah who is going to discuss autonomic nervous system function catakolamine synthesis and breakdown. Dr. Elijah has background as an assistant director and has been a dedicated educator since joining the academic faculty in 2001. He later became head of clinical in 2009. He earned his BSN from California State University in 1991, his master's from Kaiser Permanente School of Anesthesia in 1996, and his doctoral degree from Pepperdine University in 2005. His teaching and research interests include cardiac anatomy, physiology, pediatrics, adult education, and clinical evaluation. Dr. Elijah has served as a director with Council on Accreditation, the COA, and was recognized as a fellow of the AA in 2021. who remains a dedicated educator and is the founder of the nurse anesthesia.com, a leading educational resource for IC nurses and nurse anesthesia residents. Be sure to check it out. Without further ado, let's get into today's show. Hi, CSPA listeners. My name is Sass El Salisha and I'm one of the members of the nurse anesthesia. We like to call it TNA. And I'd very much like to thank Jenny and Michelle for allowing me to speak to you today. We're going to talk all about the autonomic nervous system. And as we like to say at TNA, it is go time. The autonomic nervous system is one of the most important things for you to understand because as you're providing anesthesia, general anesthesia, many times, most often, the only thing that you're going to see in order to be able to determine the light lightness or depth of the patient in terms of their anesthesia plane is by looking at the autonomic nervous system. One great thing about the autonomic nervous system, the trends follow themselves over and over. So for instance, let me give you an example. During intubation, many times our patients become mildly hypertensive and tacocartic. Why? Because we're intubating them and putting a breathing tube in them. Sometimes during the anesthetic procedure, surgeons may not be doing anything stimulating. If we do not decrease the depth of our anesthetic, all of a sudden the patient may become hypotensive. So what we were looking at in the first example is sympathetic nervous system stimulation or parasympathetic nervous system inhibition. And as the patient is deep without surgical stimulation, if we don't titrate our medicines down, the patient all of a sudden becomes hypotensive parasympathetic nervous system predominance. So knowing the autonomic nervous system is incredibly important for you to make informed decisions as you're caring for your patient during an anesthetic. Let's take a look at our objectives or essential knowledge for this brief talk. We're going to discuss the components of the central nervous system and peripheral nervous systems. We're going to identify the significance of the autonomic nervous system in terms of anesthesia management. And I just mentioned a little bit of that to you. We're going to compare and contrast the physiologic effects of receptors. Eventually, you're going to learn all about pharmarmacology in an anesthesia way, which is in significantly more depth than probably you understand it right now. So, we're going to talk a little bit about adronurgic receptors and also muscerinic receptors, which are the receptors of the parasympathetic nervous system. And then last, we're going to discuss signs and symptoms associated with sympathetic and parasympathetic nervous system predominance. So put your seat belts on cuz here we go. So now let's take a look at the nervous system comparing both the central nervous system and the peripheral nervous system. So you guys already know the central nervous system is composed of the brain and the spinal cord. Wherever you are in terms of the body where the surgeon is doing surgery, there are sensory receptors, the sensory information via either the skin or via organs, pressure on organs or cutting organs. That information then moves up aerently to the brain and then is interpreted in the brain. The response moves in an eerent way from the brain to the periphery. Think about general anesthesia for a second. Your new job in life is to put enough anesthesia in someone's brain that you inhibit the sympathetic nervous system response. That's what you're doing during general anesthesia. The input is still coming into the brain by giving lots of anesthetic medication. What you're doing is inhibiting the brain's response to that data or to that sensory information that's coming to it. All right, let's look at the peripheral nervous system divided into two. Now, we're really not going to spend a lot of time today speaking about the sematic nervous system, but when we speak about it specifically, it has to do with the control of our muscles. So, muscles, skeletal muscle specifically. But today, we're going to talk about the other part of the peripheral nervous system, which is the autonomic nervous system. And what you'll notice is is that it is control of glands and smooth muscle. Many of which you have no voluntary control over. The autonomic nervous system very much as you know is divided into two. Sympathetic and parasympathetic. So sympathetic the an example is if you're running from a tiger. Think about what your body is doing in order to compensate. If you're actually running from a tiger, you're terrified. Your muscles are going to be working. Your heart is going to be moving as fast as it can in order to get blood to those muscles. You're going to be breathing in and out really fast because as you're using those muscles, you're building up CO2 and those muscles need oxygen in order to create cellular energy so that they can work. One last thing, think about my eyes. my pupils are going to dilate in order to get all of the light into my eyes so that I can make a judgment as to where I want to run. The sympathetic nervous system and parasympathetic nervous systems again like I said if there's one true thing that never changes in anesthesia it is how the body reacts to surgical stimulation. So if you know these effects, and this is important, you can make predictions about what is going to happen and what is happening to the patient while they're anesthetized as compared to being reactive, meaning blood pressure goes up, heart rate goes up, and now all of a sudden you're chasing those hemodynamic variables. Last parasympathetic nervous system. The example, sleep. When you're asleep, your heart rate's low, your blood pressure is low, and you have parasympathetic nervous system predominance. One last thing, between these two systems, there's a ying and yang or a balancing effect. When someone is stimulated, we have sympathetic nervous system predominance, parasympathetic nervous system inhibition, and the opposite. And that's the way we kind of like to talk about in terms of anesthesia. So, let's put this a little more into practice. going to take a look at some more anatomy and physiology. All right. Now, let's take a look at the organization of the sympathetic and parasympathetic nervous system as we're looking at it through the central nervous system. That is the brain and the spinal cord. So, as you notice in the picture on the left, we are talking about the sympathetic nervous system. You'll notice that we have the spinal cord which then we have nerves moving out in the thoracco lumbar region which is T1 through L2 and going out to the ganglia having a syninnapse and then other nerves moving to particular organs. This is the sympathetic inputs to those particular organs via the thoracco lumbar region T1 through L2. And you will learn this when you get into anesthesia school. These are questions that ends up on your boards. People will ask you in clinical. So again, the ying and yang, the balancing effect is a parasympathetic nervous system. Notice in terms of the PNS, it doesn't tremendously use the spinal cord. Yes, there's the distribution of the parasympathetic nervous system, the sacral nerves, and there's cranial nerves three, seven, and nine, which are also important. But 80% of all parasympathetic nervous system interervation to your entire body for the most part your thorax. So your chest and your abdomen come from the vagus nerve. Notice that it has nothing to do with the spinal cord. It comes out right from the base of the brain or the medulla. All right. And then one last thing just quickly on this. Think about a spinal cord injury. Think about what happens if a spinal cord injury occurs. What happens to the patient? They become bradaartic. They vasoddilate. So they become hypotensive and they also lose heat. Why is that happening? Well, you can make a case for it looking right at this picture. If a spinal cord injury occurs all and certainly if it's high enough above the thoracco lumbar region all of that sympathetic nervous system intervation is not going to work because there are no eerant signals coming down the cord and being able to then communicate with those organs. What do you have parasympathetic nervous system predominance? Why? because the vagus nerve doesn't utilize the spinal cord for its intervation. So now you know why in spinal shock or neurogenic shock patients become bradaartic they vasoddilate they lose their systemic vascular resistance and they lose heat. As they vasoddilate they lose heat to the environment. Okay let's look at this a little further again differentiating between sympathetic nervous system and parasympathetic nervous system intervation. So when we talk about the sympathetic nervous system, the major neurotransmitter of the sympathetic nervous system is norepinephrine all day long. The effects are adinuric. So we're going to talk about adinuric receptors. And when we talk about norepinephrine or dopamine or epinephrine as we'll get to, we're talking about an adinuric response that works on an adinuric receptor. What we say is the overall effect is sympathomimedic meaning mimicking the sympathetic nervous system. Example, I give epinephrine to someone. What's going to happen? Their heart rate and their blood pressure is going to increase. That is an SNS response. All right, let's look at the parasympathetic nervous system on the right hand side. So the neurotransmitter always of the parasympathetic nervous system is acetylcholine. The effect is cholineergic effect. Acetylcholine the effect is a choloneric effect. And there's another term called colonolimetic. If acetylcholine is the neurotransmitter of the parasympathetic nervous system and it is and it causes a chonergic response just like sympathylimetic mimicking the sympathetic nervous system a colon mimetic effect increasing the amount and effect of acetylcholine is going to cause a parasympathetic nervous system effect or intervation and as a result we have parasympathetic nervous system predominance. Let me give you one example. You guys give atropene, right? What does atropene do? Atropene is an anti-olonergic drug. And we most often give it to increase someone's heart rate. It makes sense. If acetylcholine is a neurotransmitter around the heart related to the parasympathetic nervous system, it can cause brada cardia. Now if we come along and give an antiolineric antagonize the effects of acetylcholine what will we get an increased heart rate. So again knowing your autonomic nervous system is really important not only to understand what's going on with the patient but also because of pharmarmacology. All right. Now let's speak specifically about the anatomy related to sympathetic and parasympathetic nervous systems. So let's look at the diagram first. Let's look at the very top. So it says there we have the first ganglion coming out of the medulla. There's your vagus nerve. Remember 80% of the parasympathetic nervous system interervation to the heart. What you'll notice in all of these pictures when you talk about nerve to post ganglionic neuron with the exception of and and including actually the adrenal gland. The adrenal gland is specific. We'll get to it in a second. When we talk about pre-toost pre gangleionic to post the neurotransmitter whether it's sympathetic or parasympathetic is always acetylcholine always acetylcholine. What differs is what happens post gangleionic second neuron to a particular organ system. So let's take a look at the first parasympathetic. We have preacetylcholine being released post gangleionic neuron. And if we're talking about the heart and also to blood vessels, we're talking about muscerinic receptors. Acetylcholine binds to muscerinic receptors and has a parasympathetic nervous system effect in the heart and then also the vessels. So, as you guys know very well, alpha and beta receptors, which we're getting to next, those are adinuric receptors, the cononergic receptor is known as a muscerinic receptor. Let's continue to move down. As we move from the parasympathetic nervous system, we are now using the spinal cord, which is denoted here in orange. Again, spinal cord, sympathetic nervous system, the raco lumbar distribution. We have spinal cord pre-neuron communication in that first ganglia is always acetylcholine. I've meant to say that about four more times. Then we have sympathetic nerve and if we have the heart and the vessels opposite of what we just talked about the neurotransmitter that is the main neurotransmitter of the sympathetic nervous system is norepinephrine and that is going to interact with an adinuric receptor. Alpha receptors if we're talking about blood vessels, beta receptors, specifically beta 1 if we're talking about the heart. Next, it's kind of weird. It's the only exception. You'll notice that it is a sympathetic fiber, but it's sympathetic. And these are the only two places that this occurs in the body. still spinal cord pre to post in terms of ganglia the neurochemical acetylcholine that has not changed but what has changes acetylcholine post to muscerinic receptor it's still termed and you would think it would be termed parasympathetic response but it's not it's termed a sympathetic coneric response this only occurs to two organ systems and that is sweat sweat glands and some small peripheral vessels. Overwhelmingly, in terms of the systemic vascular resistance, it's almost completely the sympathetic nervous system, but again, it's something that is unique within the autonomic nervous system. Let's take a look at one other thing cuz norepinephrine always gets all of the notoriety is the one that is famous. who walks into the party behind norepinephrine and that's his cousin dopamine here. So again we have three neurochemicals of the sympathetic nervous system. Norepinephrine, epinephrine and dopamine. Here's an example of dopamine and we know pre to spinal cord pre to post is acetylcholine. And notice this is a sympathetic dopamineergic neuron. It's going to release dopamine postsaptically. Specifically, if we're talking about tissue beds, look at the renal system. We know the dopamineergic receptors there and it will have a particular effect at causing vasoc constriction certainly in higher levels, right? And then last, I said the adrenal glands are unique and they are. They're kind of our turbo boosters for the sympathetic nervous system. So pre acetylcholine but notice this there is no post ganglionic nerve there is only the adrenal gland. The adrenal gland is the only place in the body that acts as its own post gangleionic neuron. Catakolamines are created in the adrenal gland and then released directly into the blood that will have an effect on both alpha and beta receptors. You'll notice that both norepinephrine and epinephrine are created in the adrenal gland. Let's take a look on the right just to kind of summarize because I went over a lot of stuff. So pre gangleionic to post gangleionic is always conuric. Whether you're talking about sympathetic or parasympathetic nervous system, it doesn't matter. When we talk about post synaptic nerve to organ, we've already mentioned this SNS major chemical norepinephrine but could be epinephrine and also could be dopamine. PNS is alwaysergic because the neurotransmitter is acetylcholine. Last are adrenal glands. This is important information for boards and for tests. The adrenal gland, the adrenal medulla creates catakolamines. And this is the concentration or difference. 80% of the catakolamines created are norepi. 20% is epinephrine. This is crazy. I didn't know this either. Epinephrine really is only created in the adrenal gland and a small number of adinuric nerves in the brain. really epinephrine the majority of it comes from the adrenal gland the adrenal medulla. So kind of interesting. Now let's take it one step further looking at sympathetic and parasympathetic nervous systems and the adrenal medulla all together on one particular diagram. We're looking at pre gangleionic neuron the ganglia which we know you'll notice all the way across acetylcholine right is that neurotransmitter from pre gangleionic to post gangleionic we have the aector neurotransmitter primarily norepinephrine in the sympathetic nervous system parasympathetic nervous system is acetylcholine norepinephrine binds to adinuric receptors in terms of the parasympathetic nervous system. Acetylcholine binds to muscerinic receptors and has an effect. So let's take a look. Let's start on the right. Parasympathetic nervous system. Acetylcholine right there in pre- to post nerve. Post nerve the choneric effect. Acetylcholine binding to muscularenic receptors. What's it going to do to the heart? What is a parasympathetic nervous system response to the heart? If parasympathetic intervation is greater than sympathetic, such as someone sleeping, you're going to get a decreased heart rate, decreased cardiac contractility, decreased rate of cardiac conduction, and lots of other effects. But in anesthesia, we're most concerned about the heart, right? So, all of our medications that we give affect the heart. And what are we looking at during a general anesthetic? We're making huge decisions related to the patients related to blood pressure and also their heart rates. All right, let's move over to the sympathetic nervous side. So, here are our sweat glands. I'm on the most right of the sympathetic. Here are our sweat glands. Here is what is unique is that even though this is a sympathetic nervous system distribution, what is unique is that it releases acetylcholine bind to a muscular receptor and again only on these sweat glands and very small peripheral veins and arteries. Where does the sympathetic nervous system where does it really earn its money? It earns its money right here. So again, pre to post acetylcholine. I've said that eight times, so you should be very aware of that. Now, and you should never forget that. Look what's coming out. Norepinephrine. Norepinephrine has an alpha effect and also a beta effect. And it is going to have the opposite effects of the parasympathetic nervous system when we talk about the heart and we also talk about vascular resistance. increasing heart rate, increasing the contractility, increasing the rate of cardiac conduction, and of course vasoc constriction is going to occur and that's going to help bring your blood pressure up. Last, just to review, adrenal medulla, it acts as its own post gangleionic neuron. It does create epinephrine, but also norepinephrine. And do you remember the amounts, the percentage amounts? Think about it for a second because we will review it at the end of the talk. It's going to go into the blood and bind to an adinuric receptor, alpha and beta receptors. The last part to this is what is the physiologic effect and that's really important. That's really what we care about. So just so you know there are enormous distributions of alpha receptors, beta receptors and also muscerinic receptors all over the body. But in terms of anesthesia, we really like to think about it in terms of the heart and also in terms of the vascule because that's what we're making the decisions to titrate our anesthetic medications to. What's the blood pressure? What's the heart rate? Or if someone is losing blood slowly, what's going to happen? As the patient compensates, the heart rate and blood pressure are going to be increased. So a sympathetic response may not only be from one single event like intubation but also may be a graded response gradual becoming more and more as someone starts to lose blood as that patient compensates. Which is why I told you one of the most important things you can do in terms of being a detective in the operating room to be proactive is to know about what the effects of the sympathetic and parasympathetic nervous system are. When we talk about alpha receptors in anesthesia, we're primarily talking about the vasculature because we care about vascular resistance. And what's going to happen when you have alpha 1 agonism or stimulation? you're gonna have vasoc constriction which is going to bring the blood pressure up. How about beta 1 effects? For the most part, beta 1 effects or beta 1 receptors are distributed only in the heart. Actually, there are beta 1 receptors in the kidney, but that's another lecture. But for today, we're going to say only the heart. What is going to happen when you have agonism? Sympathetic nervous system stimulation of a beta 1 receptor greater than a muscerinic receptor stimulation. Sympathetic nervous system predominance. And you can see the functions. Beta 2. They're beta 2 receptors all over the body, but we're really concerned about beta 2 receptors most often in the lungs because you know what do you do for someone who has asthma? Well, one of the drugs that they take chronically many times is albuterol. How does albuterol work? Well, albuterol is a beta 2 agonist. Look at the effects in the lungs. Beta 2 agonism is going to cause bronco dilation. Why do you need to know about that? Patients during anesthesia at times intubated or not can develop a bronospasm. You're going to need to know and be able to treat that. So one of the ways we treat that is with a beta 2 agonist like albuterol. Um in terms of the vascule yes there is some beta 2 dilating effects and again that's more complicated and for another time in another lecture. Last here's our parasympathetic nervous system input and that's all over the body but specifically for us for our heart and our lungs. It does the opposite of beta 1 effects and beta 2 effects. So again, there's a constant ying and yang between sympathetic and parasympathetic in order to maintain homeostasis. All right, you know this. Now, here's some of when you answer. So, which is the primary catacolamine that mediates sympathetic nervous system activity? You know this, of course, it's norepinephrine. All right. Norepinephrine has greater alpha 1 effects as compared to beta 1 and beta 2 effects. Epinephrine has greater beta effects as compared to alpha 1 effects. Now, if some of you are thinking that's not true, it is. If you give enormous doses of norepinephrine or epinephrine, the alpha 1 effects are going to predominate. In addition, with epinephrine, patients are going to get incredibly tacocartic. But under normal conditions or even a slow infusion, that's the way it works. Norepinephrine, greater alpha 1 as compared to epi greater beta 1 effects. All right, so who cares, right? Why is this information important? Think about this. You guys know you guys are taking care of patients. What is the vasopressor of choice in septic shock? What is the problem? There are lots of problems with septic shock. And what is causing it is the whatever the sep source of sepsis is. But why are you starting the patient on a drip? Because they have a loss of vascular resistance. What is one of the main drugs or the drug of choice to combat this? It's norepinephrine because of the alpha predominant alpha 1 effect. All right. Drug of choice for severe bronco spasm. Really severe. You know this. And especially with someone with allergies, what's the drug of choice? Epinephrine. Why? Epinephrine has a greater beta effect. Specifically, yes, beta 1, but also in this particular example, beta 2 to cause bronco dilation. So, you may ask yourself, why is this information vitally important for you to understand in terms of the autonomic nervous system? So, as we've talked about, it's the only thing that you can assess during general anesthesia. I always say this to my students, the body always tries to return itself to normal. It always tries to maintain homeostasis. So, if you can figure out what the body is doing and why it is doing it, specifically the autonomic nervous system, you can be proactive in terms of the things that you're treating as compared to being reactive. And we all want to be proactive. Many of the anesthetics have an inhibitory effect on the sympathetic nervous system causing the myioardium to be depressed causing vascular dilation and causing hypotension. Which is why in anesthesia most often we live our lives on the hypotensive side. The material that I went over and much more and in greater detail are going to be on exams that you're going to take in the anesthesia school and are also going to be on the national certifying exam or NCE. And then of course it's kind of cool, right, to say words like sympathetic receptor. And of course, when you know what those are, it makes you sound pretty smart, which always impresses people in the operating room. All right. So this is all you. Let's see what you learn. When stimulated, which adinuric receptor causes an increase in vascular resistance? A beta 1 receptors, B beta 2 receptors, C muscularenic receptors, and D alpha 1 receptors. And the answer is there. We are D alpha 1 receptors. Here is our next question. Which neurotransmitter within the autonomic nervous system is released from pre gangleionic nerves? You got this all day. This is easy now for you. So, A, norepinephrine, B, dopamine, C, epinephrine, or D, acetylcholine. And the answer is D as you know now or maybe before acetylcholine. All right, my friends, it is time to wrap this up. So let's do a summary of the key points. Autonomic nervous system is composed of the interplay or ying and yang effects between the sympathetic and parasympathetic nervous systems. On the adinuric side on the SNS side we have three neurochemicals norepinephrine which is the primary neurotransmitter of the sympathetic nervous system. Epinephrine and also dopamine. Alpha one agonism is going to increase vascular resistance. It's going to increase blood pressure. That's why you give a drug like epinephrine or norepinephrine to increase someone's blood pressure. Beta 1 agonism or stimulation is going to cause an increased heart rate, contractility, and rate of cardiac conduction. I'm going to pull down to number three and look at a. What are the cardiac effects of the parasympathetic nervous system? They are opposite of what I just said in B. And then last, and I titled it A, and I'm not sure why, but that's okay. I do know it should be C just in case, we have beta 2 agonism. And beta 2 agonism, as we've talked about, bronco spasm. We can give a drug like albuterol or if the bronospasm is so severe that we can't ventilate, our emergency drug is to give epinephrine. Why? because of the predominant beta 2 effects which are going to cause bronco dilation and we know the parasympathetic nervous system the receptors that are used are muscularinic receptors and the neurotransmitter of the parasympathetic nervous system is acetylcholine here is a reference for you it is one of the core textbooks in nurse anesthesia it is called nurse anesthesia two of us me Jeremy Heiner are editors in addition to our mentor John Nagelhout who actually created started the book all our editors in the book and are all contributors. John wrote the chapter on autonomic nervous system pharmarmacology and if you have a second check it out cuz he was certainly a masterful writer. Okay, who are we? Who is the nurse anesthesia or TNA? It's these three goons right in front of you. So I'm standing in front of in the middle and actually Mark is on my left hand side, Jeremy on my right and they were actually students of mine. So I am thrilled to be starting this company with them. Our main goal, and it always has been since I started and since they also started teaching, is to truly improve patient care, is to educate anesthesia people, educate ICU nurses, ER nurses, or whoever wants to listen to help gain knowledge, gain comprehension, and be able to apply that information. It's really important stuff. if I just drone on about information that you can't use in the operating room. My philosophy has always been what's the point of it. So, we're really trying to make education useful things that you can use and to take care of patients in a competent way. We have been working really hard. We are very proud to have put out our first series. It's a crisis management series and it's for everybody. It is not anesthesia specific. You can look on the right hand side and see all of the different crisis managements that we're looking at. It not only talks in a case-based format about what the case is, but also a little bit about the physiology and the treatment. So, for instance, look at number eight, hypoxia. Doesn't matter where you work in a hospital, hypoxia, uh number seven, hypotension, they are certainly things that are going to happen to your patients. Here we are in terms of our crisis management series. And if you go to our crisis management series and you decide to buy it, um, if you put in the code TNA50, you will get 50% off of the purchase price for a limited time. So, we really hope that you would consider it and maybe find it valuable. And if you do, telling others would be a great way to help us grow. We also have a free podcast. We call it the Nurse Anesthesia podcast. We've been podcasting for over a year. We have many different topics that we talk about. Some of them are listed here. We do Q&A episodes, especially geared towards students with a rationale as to why the correct answer is correct. We talk about clinical topics, pharmarmacologic topics, and certainly the airway, which is a big thing that you're going to learn about in anesthesia school. So, if nothing else, take a listen to one of our podcasts, see if you like it, and if you do, again, use that information to improve the care that you provide, and maybe tell a friend about it. So, as I mentioned, here at the nurse anesthesia, we are trying to build a community of learning in anesthesia and critical care. And that's what's most important to us, high quality learning and the ability to utilize that information in terms of the amazing things that you do for patients every single day. We created these crisis checklists. There are many crisis checklists out there. We suggest that you use them. They have been shown in related to studies and we believe that they help in terms of standardizing treatment for patients in a crisis situation. Here is the table of contents for our checklist and you'll notice that they are not only anesthesia specific. These can be used anywhere. In addition, we're going to be putting them up on our website for free and you can download them for free and share them. We would love to hear your comments and thoughts about them and any suggestions for improvement that you would have. Here's an example of one of our checklist. This happens to be anaphilaxis. All of our checklist looks similar to this. There's always a brief mechanism of action. We then talk about management and management is always in the red. So, what do I need to do now in order to stabilize that patient? If I don't know the primary diagnosis, I can look at signs and symptoms in the orange box. And last, we can look at if it's not anaphilaxis, but it looks like it was, what else could it be? What else is causing the problem with the patient? So, all of our checklists look exactly like this. One last example, no pun intended, is last local anesthetic toxicity. So we always have management in big and bold. So our primary actions, what are we going to do now for the patient? We always have a medication section with things that are with calculations that are ideally most easily read in an emergency that you can carry them out quickly. And then also again our signs and symptoms and differential diagnosis box. A checklist is only as good as you have made the correct diagnosis. And if that's not enough crisis management for you, we actually came out with a pocket book that you can use and take with you in any unit and walk around with it in the scrub pocket. So it's our emergency management anesthesia and critical care book. Provides a little bit more information in terms of the symptomatology and gives you complete lists related to differential diagnosis. You can check it out on Amazon. My name is Sass El Salisha and I'm one of the team members of the nurse anesthesia or TNA. Our website is at the bottom, the nurseanesthesia.com. Please check us out. It has been my pleasure to speak with you for the last 40 minutes. I hope you learned something and I wish you the best in your anesthesia career and hopefully I'll get to talk to you again in the near future. You take care. Bye-bye. Thank you for tuning in. Be sure to head over to sneakprepacademy.com to gather free resources to help you on your CRNA journey. Stay strong. We're rooting for you, future CRNA. [Music]