Autonomic Nervous System Function and Catecholamine Synthesis Breakdown with Dr. Sass Elisha, The Nurse Anesthesia

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Have you ever wondered why your patient becomes tachycardic during intubation—or hypotensive when the surgeon hasn’t even made an incision yet? These aren’t just random fluctuations. They’re signals from the autonomic nervous system—and as a future CRNA, being able to interpret them can mean the difference between chasing vital signs and anticipating them.

If you’re serious about anesthesia, understanding the autonomic nervous system (ANS) isn’t optional—it’s essential. The ANS influences everything from anesthetic depth to hemodynamic management, and mastering its functions gives you a clinical edge both in school and in the OR.

Here’s what you’ll learn:

• The difference between the sympathetic and parasympathetic nervous systems

• Why understanding ANS function is crucial for interpreting anesthetic depth and hemodynamic trends

• How neurotransmitters like norepinephrine, epinephrine, dopamine, and acetylcholine influence receptor activity

• The physiology of alpha, beta, and muscarinic receptors and how they guide pharmacologic decisions

• Real-world clinical examples that connect ANS theory to intraoperative decision-making

• Why the adrenal medulla plays a key role in the body’s fight-or-flight response

• How this knowledge directly applies to your future practice and board exams

In this special episode, Dr. Sass Elisha—a nationally recognized anesthesia educator and co-founder of The Nurse Anesthesia—walks you through the complex world of the ANS in a way that’s practical, clear, and rooted in real-life anesthesia scenarios.

By the end of this episode, you’ll not only understand the “yin and yang” of autonomic balance—you’ll be able to predict and respond to patient responses like a seasoned provider. This is foundational knowledge that will serve you from the classroom to the OR.

As Dr. Elisha would say, “It’s go time!”

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Why the Autonomic Nervous System Matters in Anesthesia

Hello, future CRNA. Welcome back to CSPA podcast. We have a very special guest host episode for you today by Dr. Elisha, who is going to discuss autonomic nervous system function, catecholamine synthesis, and breakdown. Dr. Elisha has a 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. Elisha has served as a Director with The Council on Accreditation, COA, and was recognized as a fellow of the AANA in 2021. He remains a dedicated educator and is the founder of The Nurse Anesthesia, a leading educational resource for ICU nurses and Nurse Anesthesia Residents. Be sure to check it out. Without further ado, let’s get into today’s show.

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Hi, CSPA listeners. My name is Sass Elisha 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 the CSPA team 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, 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. 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 tachycardic. 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. 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 pharmacology in an anesthesia way, which will be in significantly more depth than you probably understand right now. So we’re going to talk a little bit about adrenergic receptors and also muscarinic receptors, which of the receptors of the parasympathetic nervous system.

Then lastly, we’re going to discuss signs and symptoms associated with sympathetic and parasympathetic nervous system predominance. So put your seatbelts on because here we go.

Central vs. Peripheral Nervous System

Now let’s take a look at the nervous system comparing both the central nervous system and the peripheral nervous system.

You 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 afferently to the brain and then is interpreted in the brain. The response moves in an efferent 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.

Alright, 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 somatic nervous system, but when we speak about it specifically, it has to do with the control of our muscles. So muscles, skeletal muscles 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.

Sympathetic vs. Parasympathetic Nervous System

The autonomic nervous system, as you know, is divided into two: sympathetic and parasympathetic. So sympathetic, 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, then this is important. You can make predictions about what is going to happen and what is happening to the patients 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’s 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 it in terms of anesthesia.

Autonomic Nervous System Anatomy

So let’s put this a little more into practice; we’re going to take a look at some more anatomy and physiology. Let’s 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.

Autonomic Nervous System: 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.

In the picture (video timestamp 8:39), 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 thoracolumbar region, which is T1 through L2, and going out to the ganglia, having a synapse, and then other nerves moving to particular organs. This is the sympathetic inputs to those particular organs via the thoracolumbar region, T1 through L2.

You will learn this when you get into anesthesia school. These are questions that will be 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 and the sacral nerves, and there’s cranial nerves three, seven and nine, which are also important.

However, 80% of all parasympathetic nervous system innervation 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.

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 bradycardic, they vasodilate, 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. (Video timestamp 10:23)

If a spinal cord injury occurs, and certainly if it’s high enough above the thoracolumbar region, all of that sympathetic nervous system innervation is not going to work because there are no efferent 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 innervation. So now you know why in spinal shock or neurogenic shock, patients become bradycardic, they vasodilate, they lose their systemic vascular resistance and they lose heat as they vasodilate, they lose heat to the environment.

Let’s look at this a little further. Again, differentiating between sympathetic nervous system and parasympathetic nervous system innervation. So when we talk about the sympathetic nervous system, the major neurotransmitter of the sympathetic nervous system is norepinephrine. The effects are adrenergic.

We’re going to talk about adrenergic receptors and when we talk about norepinephrine or dopamine or epinephrine as we’ll get to, we’re talking about an adrenergic response that works on an adrenergic receptor. What we say is the overall effect is sympathomimetic, 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.

Alright, let’s look at the parasympathetic nervous system on the right hand side (video timestamp 12:08). So the neurotransmitter always, of the parasympathetic nervous system, is acetylcholine. The effect is cholinergic effect. And there’s another term called cholinomimetic.

If acetylcholine is the neurotransmitter of the parasympathetic nervous system, and it is, and it causes a cholinergic response- just like sympathomimetic mimicking the sympathetic nervous system, a cholinomimetic effect, increasing the amount and effect of acetylcholine, is going to cause a parasympathetic nervous system effect or innervation. And as a result, we have parasympathetic nervous system predominance.

Let me give you one example. You guys give atropine, right? What does atropine do? Atropine is an anticholinergic 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 bradycardia.

Now, if we come along and give an anticholinergic, 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 pharmacology.

Alright, 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 (video timestamp 13:51). So it says we have the first ganglion coming out of the medulla. There’s your vagus nerve. Remember, 80% of the parasympathetic nervous system innervation to the heart.

What you’ll notice in all of these pictures when you talk about nerve to postganglionic neuron, with the exception of and including actually the adrenal gland. The adrenal gland is specific, we’ll get to it in a second; when we talk about pre to post, preganglionic to post, the neurotransmitter, whether it’s sympathetic or parasympathetic, is always acetylcholine.

What differs is what happens postganglionic, second neuron to a particular organ system. So let’s take a look at the first parasympathetic. We have pre, acetylcholine being released, post, ganglion neuron, and if we’re talking about the heart and also to blood vessels, we’re talking about muscarinic receptors. Acetylcholine binds to muscarinic 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 adrenergic receptors. The cholinergic receptor is known as a muscarinic 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, thoracolumbar distribution, we have spinal cord pre neuron communication in that first ganglia is always acetylcholine. 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 adrenergic receptor. Alpha receptors if we’re talking about blood vessels, beta receptors, specifically beta one, 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 cholinergic. 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 changed is acetylcholine post two muscarinic receptor, it’s still termed and you would think it would be termed parasympathetic response, but it’s not. It’s termed a sympathetic cholinergic response. This only occurs to two organ systems and that is sweat glands and some small peripheral vessels.

Overwhelmingly in terms of systemic vascular resistance, it’s almost completely the sympathetic nervous system. But again, it’s something that is unique within the autonomic nervous system.

Understanding Catecholamines: Norepinephrine, Dopamine, and Epinephrine

Let’s take a look at one other thing because norepinephrine always gets all of the notoriety, it is the one that is famous but who walks into the party behind norepinephrine? That’s his cousin dopamine.

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 spinal cord, pre depose is acetylcholine. And notice this is a sympathetic dopaminergic neuron. It’s going to release dopamine postsynaptically.

Specifically if we’re talking about tissue beds, look at the renal system. We know there are dopaminergic receptors there and it will have a particular effect at causing vasoconstriction, certainly in higher levels, right? And then lastly, 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 postganglionic nerve. There is only the adrenal gland.

The adrenal gland is the only place in the body that acts as its own postganglionic neuron. Catecholamines 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 (video timestamp 18:44) just to kind of summarize because I went over a lot of stuff. So preganglionic to postganglionic is always cholinergic. Whether you’re talking about sympathetic repair or sympathetic 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 always cholinergic because the neurotransmitter is acetylcholine.

Lastly, our adrenal glands, this is important information for boards and for tests. The adrenal gland, the adrenal medulla creates catecholamines and this is the concentration or difference. 80% of the catecholamines created are norepi, 20% is epinephrine. This is crazy and I didn’t know this either. Epinephrine really is only created in the adrenal gland and a small number of adrenergic 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 (video timestamp 20:01). We’re looking at preganglionic neuron, the ganglia, which we know you’ll notice all the way across, acetylcholine, is that neurotransmitter from preganglionic to postganglionic.

We have the effector neurotransmitter, primarily norepinephrine in the sympathetic nervous system. Parasympathetic nervous system is acetylcholine. Norepinephrine binds to adrenergic receptors. In terms of the parasympathetic nervous system, acetylcholine binds to muscarinic 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 cholinergic effect, acetylcholine binding to muscarinic receptors.

What’s it going to do to the heart? What is a parasympathetic nervous system response to the heart? If parasympathetic innervation 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.

Autonomic Nervous System: Looking at sympathetic and parasympathetic nervous systems and the adrenal medulla all together on one particular diagram

Alright, let’s move over to the sympathetic nervous side. So here are sweat glands. I’m on the most right of the sympathetic (video timestamp 21:42). Here are 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, binding to muscarinic 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 vasoconstriction 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 postganglionic 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 adrenergic receptor, alpha and beta receptors.

Muscarinic and Adrenergic Receptors

The last part to this is, what is the physiologic effect? And that’s really important. That’s really what we care about. Just so you know, there are enormous distributions of alpha receptors, beta receptors, and also muscarinic 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 vasculature 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. 

This 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.

What’s going to happen when you have alpha one agonism or stimulation, you’re going to have vasoconstriction, which is going to bring the blood pressure up. How about beta one effects? For the most part, beta one effects or beta one receptors are distributed only in the heart. Actually there are beta one 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 one receptor greater than a muscarinic receptor stimulation, sympathetic nervous system predominance. And you can see the functions (video timestamp 25:13).

Beta two- There are beta two receptors all over the body, but we are really concerned about beta two 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 two agonist. Look at the effects in the lungs. Beta two agonism is going to cause bronchodilation. Why do you need to know about that? Patients during anesthesia, at times intubated or not, can develop a bronchospasm. You are going to need to know and be able to treat that. So one of the ways we treat that is with a beta two agonist like albuterol. In terms of the vasculature, yes there is some beta two 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 one effects and beta two effects. So again, there’s a constant yin and yang between sympathetic and parasympathetic in order to maintain homeostasis.

Alright, you know this. Now here’s where you can answer. So which is the primary catecholamine that mediates sympathetic nervous system activity? You know this, of course it’s norepinephrine. Alright? Norepinephrine has greater alpha one effects as compared to beta one and beta two effects.

Epinephrine has greater beta effects as compared to alpha one effects. Now, if some of you were thinking that’s not true, it is if you give enormous doses of norepinephrine or epinephrine, the alpha one effects are going to predominate. In addition with epinephrine, patients are going to get incredibly tachycardic, but under normal conditions or even a slow infusion, that’s the way it works. Norepinephrine, greater alpha one as compared to epi, greater beta one effects.

Autonomic Nervous System Knowledge for Clinical Decision-Making

Alright, so who cares, right? Why is this information important? Think about this. You guys know, you 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 whatever the 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 predominant alpha one effect. Alright, drug of choice for severe bronchospasm, 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 one, but also in this particular example, beta two to cause bronchodilation.

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 myocardium 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 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 sympathectomy or muscarinic receptor. And of course when you know what those are, it makes you sound pretty smart, which always impresses people in the operating room.

Alright, so this is all you, let’s see what you learned: When stimulated, which adrenergic receptor causes an increase in vascular resistance? A, beta one receptors. B, beta two receptors. C, muscarinic receptors, or D, alpha one receptors. And the answer is: D, alpha one receptors.

Autonomic Nervous System: 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.

Here is our next question. Which neurotransmitter within the autonomic nervous system is released from preganglionic nerves? You got this all day. This is easy now for you. Is it A, norepinephrine. B, dopamine. C, epinephrine or D, acetylcholine. And the answer is D, acetylcholine. Alright 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 yin and yang effects between the sympathetic and parasympathetic nervous systems. On the adrenergic 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 one 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 (video timestamp 31:36), 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 entitled 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 two agonism and beta two agonism as you talked about bronchospasm, we can give a drug like albuterol or if the bronchospasm is so severe that we can’t ventilate, our emergency drug is to give epinephrine. Why? Because of the predominant beta two effects which are going to cause bronchodilation.

And we know the parasympathetic nervous system. The receptors that are used are muscarinic receptors and the neurotransmitter of the parasympathetic nervous system is acetylcholine. Here’s 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 started the book. We are all editors in the book and are all contributors. John wrote the chapter on autonomic nervous system pharmacology and if you have a second, check it out. He was certainly a masterful writer.

The Nurse Anesthesia

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 in the middle (video timestamp 33:05) and 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?

We’re really trying to make education useful, things that you can use 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. 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, hypoxia. Doesn’t matter where you work in a hospital. Hypoxia. Or 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, if you put in the code TNA50, you’ll 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. 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, pharmacologic 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.

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 related to studies and we believe that they help in terms of standardizing treatment for patients in a crisis situation. Here’s the table of contents for our checklists (video timestamp 36:30), 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 checklists. This happens to be anaphylaxis. All of our checklists look 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 anaphylaxis, 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 reactions, what are we going to do now for the patient? We always have a medication section with calculations that are ideally most easily read in an emergency that you can carry them out quickly. And then also, again, are 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 pocketbook 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 in Anesthesia and Critical Care book. It provides a little bit more information in terms of the symptomatology and gives you complete lists to differential diagnosis. You can check it out on Amazon.

My name is Sass Elisha and I’m one of the team members of The Nurse Anesthesia or TNA. Our website is TheNurseAnesthesia.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. Hopefully I’ll get to talk to you again in the near future. You take care. Bye-bye.

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