Episode 68: Why you care about the ANS

The goal is to learn , inspire and bring Cardiopalm to the forefront of conversation . Thanks for joining me today and let's get after it . Hello , hello and welcome to today's episode of Talking All Things Cardiopulm . I am your host , Dr . Rachele Burriesci .

Today's episode is sponsored by Jane , a clinic management software and EMR that helps you handle your clinic's daily administrative tasks so you can free up your evenings and weekends . The Jane team understands how precious your time is and recognizes that charting can often be the most time-consuming administrative task for practitioners . That's why they're here to help .

To save you from having to start your notes from scratch , you can check out Jane's template library , which gives you access to templates that have been generously created and shared by health and wellness practitioners in the community .

Once you have the template that you like , you can choose to customize it further with charting tools such as range scales , text fields , check boxes and much more , to see how Jane can help you spend more time doing what you love . Head to the show notes to book a personalized demo .

Or , if you're ready to get started , you can use the code CARDIOPALM1MO at the time of signup for a one month grace period applied to your new account . Thanks again , jane . All right , welcome back . I hope everyone had a happy 4th . Hope everyone had a safe , healthy , fun holiday weekend .

I think July 4th weekend , or at least where it fell this time , is one of those like PTO life hacks that if you take the Friday in between you get something like five days . So we were close . Nikki and I both worked Friday , but we hosted July 4th , so we had a fun , impactful day with family . We had great weather . Literally it was in the 80s .

It was perfect temp . We were supposed to get rained out . Rain held off and I mean we could not have asked for better weather , especially since we've been like hanging in the high 100s for the past few weeks . So literally such a great turnout on weather , we ended up having the weekend off . So I was 100% surprised by this .

I thought I worked Friday to Sunday , but I checked the master schedule and I wasn't on it . So this is technically a holiday weekend . I didn't get picked for July 4th weekend so even though I signed up for it , it wasn't my weekend .

So all of a sudden I had this free weekend and I was like , oh my God , this feels so good to have a Saturday and Sunday off and be home , right Like not traveling . So we had a little bit of a lazy weekend , got some stuff done around the house , a little catching up Again , just that regular adulting type stuff .

But it was wonderful and we had such great weather . So we had like this giant or drastic change swing in weather over the past week and a half and I think the last two days we've been waking up in like the low 60s . This is crazy . So we were like 103 for about a week straight and then all of a sudden we're like low 60s in the morning , mid 80s .

I'm like this . The weather has not figured itself out here , but my garden is happy . The weather's been great . I truly can't complain . I was just sitting out on the patio getting some work done and had a impromptu summer rainstorms . That was glorious , and now we're back in .

So I wanted to jump in and talk about the autonomic nervous system today and I've thought about doing this talk a few times . I actually had to go back to see if I've already done this and I haven't . But this is a really important concept , just like at base in the world of physiology .

So if you know anything about me , I'm a giant nerd when it comes to this stuff and I truly believe that if you can understand the background knowledge , the physiology behind it all it makes the more in-depth concept so much easier to tackle . So if you can understand the basics , the foundation , everything else sort of works itself out .

So part of diving into the autonomic nervous system and just like understanding it can feel a little bit like you're diving into the weeds and we're going to get a little bit in the weeds . But I want you to understand that if you can get this concept , you're going to be able to understand medications much more efficiently .

Understand medications much more efficiently . Not all medications right , because they don't all follow the receptors within the autonomic nervous system , but a good amount . It's going to give you a nice base knowledge . I want to say something like 40 to 60% of cardiopulmonary meds can really help you out here . Another big topic is heart transplant .

So understanding the autonomic nervous system and how it works and the backup systems that are in place will allow you to understand the overall picture of a person that has a heart transplant , and we'll kind of talk about why in a bit . And the other big piece is understanding heart rate variability . And so heart rate variability is a hot topic right now .

It's a topic that I'm going to talk about , probably in the next few weeks . But I realized as I was going through some of the literature that I can't talk about heart rate variability without having this base understanding first , because everything really feeds off of this information base understanding first , because everything really feeds off of this information .

So we're going to kind of talk more about the heart versus heart and lungs , but lungs will be thrown in just a little bit . But when we're thinking about how the heart responds or how the heart works , we have to think about intrinsic and extrinsic factors .

So the coolest thing about the heart is that it comes prepped with myocardial cells that allow for automaticity , rhythmicity and conductivity . Essentially , once a heart cell fires , it is able to contract and stimulate the rest of the cells . So , in theory , the heart has the ability to function on its own .

We know that's not the case , but it has the physical capability of doing so . And so besides the cells that are involved , the heart also has a specific conductive pathway . So in a perfect world the SA node should fire the initial stimulation for the heart right .

It's that where the action potential is created and it's going to go from the SA node down the internodal path to the bundle of his , down the left and right bundle branches , to the Purkinje fibers , and then it's going to contract and the cool part about that is that we have this conductive pathway that then moves into muscular contraction .

It's such a beautiful symphony that when you start breaking it down you can't really just focus in on one thing because there's so many different aspects . So I'm going to try my best to kind of streamline this information . So the SA node is considered the pacemaker of the heart because it has the fastest depolarization rate in the heart .

It's 60 to 100 beats per minute , which , as we know , is normal resting heart rate . So , best case scenario , the SA node is what should be activating that impulse and besides it being the fastest rate of depolarization , its location is like in the perfect spot , so it's at the upper right aspect of the right atrium .

So once it fires it's going to be able to spread that electrical path down and across the heart , making for a very synchronized , efficient ringing , motion or contraction of the atria and ventricles . Of the atria and ventricles , it's just so , I don't know .

To me is so amazing to like really think about the functionality of how it works and then just how detailed and how many things are happening simultaneously to have this event occur . So in theory , the heart is considered autorhythmic , meaning it can basically create its own action potentials .

We get an influx of sodium and calcium , which creates depolarization , and an efflux of potassium , which creates repolarization , and we have this ability to contract . In theory , if you took the heart outside of the body , it would continue to contract on its own , but we know that the heart does not work independent of itself .

It is much more complicated than that . We can say that we have extrinsic factors that really play a role in that second to second , minute to minute change on the heart , and so typically we say neural , hormonal or neural endocrine is really how we have this extrinsic network that basically facilitates heart rate , heart contraction , all that stuff .

So we can get real complicated and start at the brain , and the only thing I'm going to say about the brain is that the cardiorespiratory center is at the medulla oblongata and it's broken down into cardio accelerator , cardio inhibitor and vasomotor center .

So we have these three centers that start in our medulla , in the brainstem , that basically signal out to the autonomic nervous system . So it kind of gives us some good verbiage to .

Cardio accelerator is going to stimulate the sympathetic side , cardio inhibitor is going to send signals to stimulate the parasympathetic side , and vasomotor is really going to stimulate sympathetic , to stimulate vasculature . So that's just kind of like a basic , you know higher center neural pathway . But what we're going to spend time on is the autonomic nervous system .

So the autonomic nervous system is split into sympathetic and parasympathetic , and I think a lot of people have a understanding of sympathetic and parasympathetic , even in non-health care settings . I think we're getting better about spreading or understanding the body a little bit more .

So the layman's terms that we can put on sympathetic are fight or flight , or fight and flight , and the layman's terms that we're going to put on parasympathetic is rest and digest , and so there's a lot of truth to those names , but there is more to them as well . Okay , so I'm going to like pull out some old school words .

If you haven't thought about neurotransmitters and receptors , we're going to hit them right now .

So , essentially , when we're thinking about sympathetic and parasympathetic , we do have to have names attached to the neurotransmitter and receptors that are working together , because this is what's going to help you with medications understanding what is happening at the heart , understanding what is happening at the lungs , so on and so forth .

So when we're thinking about the sympathetic system , we're going to have the neurotransmitter as norepinephrine . So norepi is our sympathetic neurotransmitter . It's going to basically send that signal out and we're going to be looking for adrenergic receptors with sympathetic system .

So when we think about adrenergic receptors , we have alpha and beta and that's further broken into alpha one and two , beta one and two . So on the sympathetic side , on that fight or flight , we have neurotransmitter norepinephrine with its adrenergic receptors , alpha-1 , alpha-2 , beta-1 , beta-2 .

Now you're probably already like oh , this is , we're in the weeds , let's pull , let's get out of the weeds . This is important , okay . One of the common statements I would tell my students is why do you care ? And there is a very big component to why you care in this situation .

So , first of all , when you hear alpha , alpha typically is related to vasculature . So if we're stimulating alpha , we're going to be stimulating vasoconstriction , typically at the vessels , the smooth muscles in the arterioles . If we hear beta one , we're stimulating the heart .

So the way I like to remember this is beta one you have one heart , so beta one stimulates the heart . Beta two two lungs . Beta two stimulates the lungs . So just an easy way , especially for my students who are potentially sitting for an exam , if you're having a hard time remembering the difference between beta-1 , beta-2 , beta-1 , you have one heart .

Beta-2 , you have two lungs .

So when we're thinking about these adrenergic receptors , we're thinking about a sympathetic system that is stimulating , right .

So we're being chased by a bear , a tiger , whatever what has to happen , for you to be successful in flight or fight , right , you're going to have to increase your heart rate , increase your blood pressure , increase your capability of breathing , bronchodilation , right ? Those are all the things that's going to be happening with a sympathetic response .

So when we're thinking specifically about beta-1 , we're going to have an increase in our heart rate . We're going to have an increase in our stroke volume . We're going to have an increase in our blood pressure . We're going to have an increase in our squeeze heart contractility , which is going to give us an increase in our cardiac output .

We also get some vasoconstriction with beta-1 . On the alpha side , think vasoconstriction as well , and the goal of vasoconstriction in this scenario is that we're going to redirect blood flow , so we're vasoconstricting where we do not need blood flow and then we are vasodilating to active working muscles .

But when you're thinking sympathetic system , you're thinking vasoconstriction , which also supports an increase in blood pressure , right . And then when you're thinking about beta two , beta two , two lungs trying to run away , what needs to happen ? I need bronchodilation .

Okay , so bronchodilation occurs at the lungs , with a sympathetic response and it does also have some vasomotor response , and so beta two is responsible for some vasodilation at the smooth muscle . So why do you care ? Right , you're like okay , we just went through these receptors . Now I have this information . Why do I care ?

I think medications is probably the easiest scenario to say why you care . First of all , if you can understand this piece , meds are so easy . Like I said , 40 to 60% . It doesn't hit all of them , but it hits a good amount of cardiopulmonary meds . That will help you easily break down the information . So one example beta adrenergic agonists .

What is a beta adrenergic agonist ? Beta adrenergic agonists are better known as beta blockers . Right , and I'm sorry , did I say that wrong ? Let me say it again , just in case Beta adrenergic antagonists Antagonist is going to be an inhibitor . Adrenergic are the receptors that we're talking about , and we're specifically talking about beta .

So we have beta adrenergic antagonist . If you have an antagonist , you're going to inhibit beta . So the easiest way to remember this is beta blocker . You're blocking beta . So , in theory , if you have a beta blocker , you want to know if it is selective or not selective .

And the reason why you want to know this is because if it's selective to beta one , then you have a more specific medication that is going to be more specific to the heart . So if you have a beta antagonist , beta blocker , everything on that beta list is going to be inhibited .

So if we know beta one increases heart rate , increases squeeze , increases stroke volume , increases cardiac output , if we inhibit that , if we block that , what is the response ? Decreased heart rate , decreased blood pressure , decreased stroke volume , decreased cardiac output . Okay , so that's just one example .

If you have a non-selective beta blocker , then you need to understand that it's not just going to affect beta-1 , it's also going to affect beta-2 . And so we said beta-2 affects the lungs and beta-2 helps bronchodilate the lungs . So if we inhibit beta-2 , we can cause bronchoconstriction .

So this is super important because if you have a patient that has lung disease and they're given a non-selective beta blocker , it can very much affect their lungs and maybe exacerbate their breathing or their shortness of air . It's a small piece of information that can make a huge difference for that person . The flip side of this is a beta-2 adrenergic agonist .

So this is a different medication class . We're saying specifically beta-2 and we're saying agonist , right , so agonist is going to support , it's going to stimulate . So what happens if we're going to simulate beta-2 ? Well , we know beta-2 causes bronchodilation . So if I stimulate beta-2 , I am going to cause bronchodilation .

Probably the easiest thing to think about with a beta-2 adrenergic agonist is a SABA , a short-acting beta-2 agonist , which is albuterol . This is your rescue inhaler . And what is the job or the mechanism of action of that rescue inhaler ? It's to stimulate bronchodilation . Okay , two examples that can very much help you on a test question and or just understand .

You know meds in the clinic , if we have something in the alpha world , so alpha adrenergic antagonists .

So if we're if we know alpha typically causes vasoconstriction and we have an alpha antagonist , then we're going to have something that causes vasodilation , and so these are meds that are typically used in the ICU setting , and one example of this is Prezosin , otherwise known as Minipress . It basically causes vasodilation , right ?

So simple information , basic , foundational in the weeds information , can give you a lot of information out in the clinic . In the weeds information can give you a lot of information out in clinic . I'm going to just say one more thing about meds in this regard , depending on the selectivity of something depends on how many receptors are effective .

So if something is not selective , you have to understand that even if you're trying to target the heart , you might get effects at the lungs and you might get effects at the vessels , and these receptors do exist in other places as well . So the more specific , selective your medication is , the more precise the response will be .

Another thing to think about are side effects . If a drug is trying to decrease heart rate , decrease blood pressure , your side effect is likely going to be the extreme of the mechanism of action . So , like , one of the most common side effects for beta blockers is hypotension . Why ? Because we're blocking beta 1 .

We're decreasing the squeeze , the contractility , stroke volume . Another issue is that it can cause arrhythmias because it's going to increase that AV delay . So you're going to be able to kind of anticipate the problem and also understand the MOA . So , sympathetic side , fight or flight .

Beta one increased heart rate , increased blood pressure , increased stroke volume , increased cardiac output , vasoconstriction to some degree . Beta two , beta two the lungs , two lungs causing bronchodilation , and an alpha is usually specific to the vasculature . Okay , one other piece in the world of sympathetic is also response to heat , thermal balance .

So we can think about heat in the setting of I am out in the heat , I'm in a sauna or I'm exercising . As I exercise , my body increases heat , right . So when we have , when our body increases its heat , the sympathetic system is going to work to keep us cool so that we can continue to do the activity .

Okay , so one of the sympathetic responses to thermal balance is to actually vasodilate the vessels of the skin to allow heat to dissipate , as well as increasing sweat gland production , because the best way for humans to decrease heat is through evaporation , which occurs when we sweat .

In the same token , we're going to have a response when our body heats up , we increase heart rate , we increase cardiac output , and so these are reasons , for instance , why you should warm up before exercise .

Because as you start to warm up literally warm up thermal balance sympathetic response is going to start to increase heart rate , increase cardiac output to prepare you for said activity . So there's lots of different avenues that we can go down .

When we're talking about the autonomic nervous system , I'm trying to kind of stay in a nice tight-knit circle , but you can very easily get pulled into different thought processes because it all sort of works together .

Parasympathetic side we're going to switch , typically known as rest and digest . I like to add recovery to that rest , digest and recovery , because there's a lot of truth to rest and digest . But I think we forget about recovery and from a student perspective , recovery's got to be on that list . So first we'll break down some of the background information .

The neurotransmitter for our parasympathetic system is acetylcholine and its receptors are considered cholinergic . So the cholinergic receptor is muscarinic . So if you hear cholinergic , it's parasympathetic . If you hear muscarinic parasympathetic , it's parasympathetic If you hear muscarinic parasympathetic .

What is interesting is that the parasympathetic , very similar to the sympathetic system , innervates the heart and it innervates the SA node as well as the atria and the AV node , but it does not innervate the ventricles . So one thing I didn't say about the sympathetic system is that it innervates the SA node , the AV node , the atria and the ventricles .

The parasympathetic does not innervate the ventricles . Hold that piece of thought . When you stimulate parasympathetic you're going to get a decrease in heart rate . You get some decrease in contraction , some decrease in stroke volume , but not as apparent as the opposite in sympathetic . And the rationale is is because it does not innervate the ventricles .

In my opinion this is a backup system . You wouldn't want innervation of the parasympathetic to the ventricles because you wouldn't want to decrease contraction so much maybe that you really decrease cardiac output . So one of the ways that the parasympathetic system helps decrease contraction is actually by a decrease in calcium influx .

So just a lot of different backup systems that work kind of side by side to make something very efficient here . So when we stimulate parasympathetic we're going to get a decrease in heart rate , like I said , some decrease in stroke volume and from the lungs perspective , we're going to get bronchoconstriction .

Okay , so a lot of the medications revolved around lungs can either be beta stimulant so beta agonist , beta two agonist is going to stimulate beta two , or it could be an anticholinergic . It's going to inhibit parasympathetic , to basically prevent bronchoconstriction . So just by having that one piece of information you can understand how anticholinergics work .

So parasympathetic is considered the dominant system at rest . It helps set resting heart rate and it helps you recover with exercise . So when you're done exercising and we're waiting for your heart rate to come back to resting levels , that's parasympathetic .

So this is part of that process or theory that say , like marathon runners or avid athletes have a lower resting heart rate , is due to parasympathetic input .

Because you are able to reset at a lower rate or come back down from an increase in heart rate more quickly , you are a more efficient parasympathetic system and there's also a lot of research that states if you were unable to recover let's say in five minutes that you do have an increase in increase rate of morbidity and mortality .

It what scenario you're in depends if sympathetic or parasympathetic is a dominant system and , as you can imagine , they both cannot be stimulated simultaneously .

As the higher brain level centers tell you , you are either cardio accelerating or cardio inhibiting , and when one is on , the other is off , and so I think that's just an easy way to kind of put some background behind that .

Just looking at some of my notes that I have on this page , if I'm missing any of my notes that I have on this page , if I'm missing any of my big points here . But I think that was my primary goal . Yep , oh , the one thing I didn't talk about .

Okay , so heart transplant when we're thinking about sympathetic , parasympathetic input , we're thinking nerve connection , and so if you have this nerve signal being sent to your heart , it's going to be a very quick response .

And if , again , we're thinking about this higher brain center , literally you can think about exercise like I'm thinking about starting my exercise routine in the next 20 minutes . If I start thinking about exercise , my brain starts sending a signal to my heart to prepare for said exercise . This doesn't happen with heart transplant .

So think about both of it , sympathetic and parasympathetic . Right , if I'm thinking about exercise , if I start exercising , if I get scared , if I'm running from a bear , if I'm nervous , what's going to happen , I'm going to have that immediate increase in heart rate to help prepare me for the activity that I'm about to do .

Right , it's almost primal , in some form Parasympathetic . True , too right , it's almost primal , in some form Parasympathetic , true too . Right , at rest , me just hanging out . Parasympathetic is my dominant system . It's maintaining my resting heart rate to be somewhere between 60 and 100 . Okay , now I have someone who has a heart transplant .

When you have , most commonly , an orthotopic heart transplant , they remove the native heart and put in the donor heart so they have to cut out the nerve fibers that were attached . So , essentially , with heart transplant you don't have that immediate connection .

Now , the coolest part about heart transplants is that they can regenerate said nerves , but it takes years and years and years . So if you don't have this normal connection , this literal connection from your brain to your heart , that immediate pathway that's going to send a signal immediately , then what happens ?

Well , your resting heart rate actually sits greater than 100 . That's number one . So your resting heart rate is higher . Why ? Because you don't have that vagal nerve to help set that lower resting heart rate . So I think that's a super cool thing . And then , number two as you start exercising , your heart rate doesn't immediately increase .

It takes greater than five minutes . Okay , so that's a huge piece of piece of information . If you're working with a heart transplant patient , you need to increase your warm up time . So we normally say warm up . A normal warm up is somewhere between five and 10 minutes For a patient with heart transplant . You want to say between 10 and 15 .

The reason is because this was the one piece I didn't get to is that you're actually now relying on the endocrine system to supply the catecholamines to the heart . What does that mean ?

That means your adrenal gland is going to be able to send epinephrine to the heart to increase heart rate for exercise , but the process of the hormones being released from the gland making its way through the blood circulation to then stimulate the heart takes longer .

So the number one thing any student or person who's prepping for CCS should know about heart transplant is that you are denervated , which means you don't have that nerve connection , and it's going to have . That patient is going to have a delay response in heart rate to activity and their resting heart rate .

It's significantly higher because we don't have that connection . I think it's phenomenal , excuse me . What I think is even more cool is that there's so many backup systems in place to accommodate this change . Accommodate this change .

So , even though my nerves are cut , my body has another way to complete the task , and so there are a number of hormones that basically stimulate and or work alongside parasympathetic and sympathetic states .

So if I need to increase my blood pressure , my adrenals also release aldosterone antidiuretic hormone , which can play with the volume in my blood and cause vasoconstriction that way with vasopressin right . So we have all of these like built-in backup systems to help accomplish one task . So if this one fails , I have this system that kicks in .

I think it's so phenomenal that sometimes you cannot wrap your whole brain around all of the things that are happening at one time . All of the things that are happening at one time , so big picture . The heart is affected by both intrinsic and extrinsic factors . Intrinsically , it can beat on its own .

We have this internal mechanical cell situation that essentially will allow the heart to continue to beat and it will typically activate from the SA node and have this nice normal rhythm of 60 to 100 beats per minute . But that is not how the system works .

It relies on extrinsic factors to accommodate for what's happening in our life and although we are no longer running from bears for the most part I mean some people might have to we have other stressors in our life . Something as simple as giving a presentation in front of 200 people , maybe getting up to bat at a big game .

There's two outs and you're the last person up and it's on you , right Like ? Whatever the situation is , there are different stressors . That's going to activate the sympathetic system . We're going to use beta-1 to stimulate the heart , beta-2 to stimulate the lungs and alpha to stimulate the vessels . That's at its base .

Parasympathetic rest and digest is going to help set our resting heart rate . It's going to use our cholinergic receptors is going to help set our resting heart rate . It's going to use our cholinergic receptors . We're going to help recover from exercise with our parasympathetic system .

And if we understand these receptors at their base , we can really tackle a large number of medications and understand them , just their mechanism of action , by understanding this information . Okay , I think that is all I wanted to cover today .

This is a good setup to get into heart rate variability and it's a good setup to talk about cardiac and pulmonary meds and it's a great setup for talking further about heart and lung transplant . So this is your foundational information , the nooks and cranny in the weeds that's going to help you break down more complex information in future conversations .

All right , I hope that was helpful for you . Reach out if you have any questions , if you got any value from this episode . Please drop me some stars . Write a great review . It is 100% appreciated . Thank you so much for being here . Thank you for listening . I hope you all have a wonderful day . Whatever you have to do , I get after it . Thank you .