Electrophysiology Explained: How Autonomic Nervous System Controls Heart Rate

all right engineers in this video we're going to talk about uh electrophysiology so if you guys are here for part two I

really appreciate it we're going to go into a little bit more detail and we're going to go over what's called extrinsic

ination of the heart so we're going to talk about we already talked about in the cardiac conduction system like the

intrinsic part of it we talked about how we set a normal sinus rhythm but now what we're going to discuss is in

certain situations how can we increase heart rate greater than the sinus rhythm and how we can we decrease the heart

rate below the sinus rhythm so that's what we're going to talk about if you guys have already watched our videos on

blood pressure regulation we talk about all how the nerves are coming out of the spinal cord or from the actual brain

stem so we're not going to go over that pathway we're just going to look at exactly how the sympathetic nervous

system and the parasympathetic nervous system affect the heart rate and then how the sympathetic nervous system

affects the contractility of the heart okay so we're going to look at some of the the actual mechanisms of this so

let's go ahe and get started if we look here I'm going to have a special receptor there this receptor is called a

beta one adrenergic receptor very very specific receptor located within the heart you can also find it on the JG

cell of the kidney too and what happens is let's say here I have a neuron here this is a sympathetic nerve right let's

say this is a sympathetic nerve and what happens is this sympathetic nerve is releasing chemicals like neuro

epinephrine and epinephrine and what happens is norepinephrine and epinephrine are going

to come over here and they're going to bind onto this beta 1 adrenergic receptor and stimulate this

receptor when this happens it activates intracellular processes like how so what it does is it first comes into the cell

and activates a g stimulatory protein okay when it activates this G stimulatory protein what happens is this

G stimulatory protein gets rid of GDP and binds GTP which turns this stimulatory protein on this stimulatory

protein then goes and activates an affector enzyme located on the cell membrane this affector enzyme is called

a denate cyclas right and what is so special about a denate cyclace if you remember we said a denate cyclas is

responsible for converting ATP into cyclicamp why is this important because cyclicamp can go and activate a special

enzyme called protein kise a why is this important because if you remember we talked about this a little

bit in the blood pressure regulation video but protein kise a can Target special protein channels you see these

green channels up there those L Type calcium channels let's say I put a small one right here on the membrane so let's

say I put these L Type calcium channels right here on the cell membrane right here so here's an L Type calcium channel

and here's another L Type calcium channel what happens is this protein KY a is going to come over here and it's

going to phosphorate these channels so it's going to put a phosphate on this channel and put a phosphate on this

channel when you put phosphates on these channels it's going to stimulate these channels to open

when these channels open guess who starts flooding in calcium when the calcium starts flooding into the

cell in Greater amounts than normal so you already going to have this calcium coming in normally because of the

intrinsic ability of the cell but then the sympathetic nervous system is going to be like hey I'm going to help you out

and I'm going to increase even more calcium coming into the cell so now you have more calcium into the cell now the

cell is going to be depolarized more frequently so what is the whole purpose of this if we bring more calcium into

the cell this cell is going to depolarize quicker so because it's going to

depolarize quicker it's going to generate Action potentials quicker because it generates Action potentials a

lot quicker when they going denote Action potentials at a APS this is going to increase the heart

rate what is it called whenever you increase the heart rate very significantly at least to a point to

where the heart rate is greater than approximately about 100 beats per minute this is referred to as tacac cardia okay

tacac cardia and tacac cardia is again the point in which there's an increased

heart rate at least point it's greater than 100 beats per minute so if the sympathetic nervous system is activated

it can increase the heart rate enough to bring the actual heart rate greater than 100 beats per minute how again phosphor

lating these L Type calcium channels to increase more calcium entry into the cell more than normal to increase the

depolarization quicker cause more frequent action potentials which increases the heart rate which causes

this uh tacac cardic effect okay which can be normal sinus Tac cardia it can happen when you're exercising okay but

now let's say that you want to slow your heart rate down okay you want to slow your heart rate down you're trying to

relax you're trying to just chill out watch some cartoons okay what's going to happen your parasympathetic nervous is

going to come on it's going to slow down your heart because we don't need to exert it we don't want to overe exert it

we just want to relax so acetylcholine is going to be released by these parasympathetic neurons right remember

that are coming from the vagus nerve and when these parasympathetic neurons they release a chemical called

acetylcholine acetylcholine binds on to these receptors present on the membrane what is this receptor here called this

receptor we said was called a M2 receptor which stands for muscarinic type 2 receptor when acetylcholine binds

onto this receptor it activates what's called called a g inhibitory protein but remember we said that g inhibitory

protein is kind of actually broken into three components Alpha inhibitory beta

inhibitory and another one which is called gamma inhibitory whenever acetum binds onto

this muscarinic receptor it activates the alpha inhibitory to separate from the beta and gamma inhibitory the beta

and gamma inhibitory come to the cell membrane and bind onto special channels in the membrane

these channels are special and specific and sensitive to the movement of pottassium

what happens is these actual beta and gamma subunit come over here and bind onto these

channels when it comes over here and binds onto these channels it causes these channels to open up and guess who

starts flowing out potassium as pottassium starts flowing out of the cell what starts happening to

the inside of the cell the inside of the cell is losing positive ions so positive ions are leaking out of the cell as

positive ions are leaking inside of the cell the cell is becoming increasingly more negative as the cell starts

becoming increasingly more negative that decreases the rate at which the the depolarization will occur it decreases

the action potentials and decreases the heart rate this effect is it's going to try to

hyper polarize the cell where the sympathetic is trying to depolarize the cell and this

hyperpolarization is going to decrease the action potential rate which is going to decrease the heart rate and if the

heart rate decreases significantly to the point where it actually goes below sinus rhythm so less than 60 beats per

minute this is going to be what's called bradicardia so whenever the heart rate is less than 60 beats per minute this is

called bradicardia okay this is called bradicardia okay so we know brat cardia and we know

tacac cardia bardia is whenever the heart rate is actually less than 60 beats per minute tacac cardia is

whenever the heart rate is actually going to be greater than 100 beats per minute what's the next thing you see

this Alpha inhibitory unit there's a specific reason for him what he does is he comes over here to this adate cycl he

comes over to the adental cycl and inhibits the idate cycl if you inhibit the Aden cyclas you inhibit the

conversion of ATP into cyclicamp what starts happening to the cyclic levels they start dropping as that starts

dropping protein KY a levels start dropping as that starts dropping it starts decreasing the phosphorilation

what is that going to do that's going to decrease the calcium entry which is going to decrease the action potential

frequency which is going to decrease the heart rate that's another way that the parasympathetic nervous system can do

this so two things one is the beta and gamma inhibitory subunit bind onto potassium iium voltage gated potassium

channels which are then going to open and potassium can flood out of the cell losing positive ions making the cell

more negative hyperpolarizing the cell and if the cell hyperpolarizes it decreases the rate at which it it

actually can generate Action potentials which decreases the heart rate and if it goes less than 60 beats per minute it's

called bradicardia another way is it can activate this Alpha inhibitory which can

bind onto a denate cyclas and con inhibit the conversion of ATP into cyclic which decreases the protein cyas

a levels decreases the phosphorilation decreases the calcium entry decreases the frequency of action potentials which

uh decreases the heart rate as a result okay that's the parasympathetic effect now who is supplying the actual

nodal cells be the parasympathetic you have to remember this is the Vagas okay you have to remember that this is the

Vagas nerve okay and then the actual sympathetic nerves are coming from the

Chang ganglia or from the superior middle and inferior cervical gangon okay so they're coming from T1 to T5 from the

Chang ganglia Superior Middle inferior cervical gangon the sympathetic fibers and the epinephrine is also released

from the Adrenal medulla sweet deal so we know how that's going to affect the heart rate how does the sympathetic

nervous system oh one more thing what is it called whenever you increase the heart rate so the sympathetic nervous

system is trying to increase the heart rate that is called whenever you try to increase the heart rate it's called

positive chronotropic action okay but then the Vagas nerve via the parasympathetic

nervous system is trying to decrease the heart rate if you try to decrease our rate that what's that called it's called

negative chronotropic action we'll talk about this in more detail whenever we get to

cardiac output but again just giving you that U relationship there now the sympathetic nervous systm also has

receptors on the contractile cells not just on the nodal cells it's a beautiful thing so now what can happen same thing

let's pretend that that actually guy over here that nerve same thing he's coming over here and he's releasing what

chemicals he's releasing neuro epinephrine and let's say that there's also the release of epinephrine from the

Adrenal medulla right so there's also Epi here these guys are going to bind on to

this what receptor it's still the same receptor the beta 1 adrenergic receptors so these are your beta 1 aeric receptors

when these guys bind they stimulate at this G protein coupled receptor which does the same function here so it's the

same action what's the overall effect here what it happens let's actually show you real quickly fastly right G

stimulatory protein here does what activates what's this enzyme here Aden cycl aenl cyclas does what converts ATP

into cyclic cyclic activates protein kinase a if protein cyas a levels increase this is where it becomes very

critical so as the protein Kye levels increase two things happen let's make this pink so that we can see how

important it is look at this the protein kyes a comes over here and he does two things one is he phosphates these

channels here on the coplas culum very special channels that consist of a special protein so one thing is he

phosphorites these channels which consist of a special protein what is this protein here called that's kind of

controlling these channels the protein here is called phospholamban okay that's a heck of a

name there sounds like you know something off of The Flintstones but like

phospho lamban okay so there's this protein called phospholamban and what happens is

when you phosphorate the proteins uh these phospholamban proteins it stimulates these channels right here you

know what this does it opens up the channels on this membrane and sucks in in a lot of calcium ions sucks a lot of

calcium ions into the sarcoplasmic reticulum what is the purpose of this if we bring a lot of calcium ions in here

we're trying to increase our cytop our um organellar storage of this calcium why is that important we're going to see

in just a second so one thing is the protein KY a phosphates the phospholamban proteins on the

sarcoplasmic reticulum sucks more calcium into the SR that has a significant purpose the second thing

that happens is the protein kise a comes over here you see these channels here these L Type calcium channels you know

how important they are again they come over here and put phosphates on these voltage gated calcium channels

what happens more calcium than normal is coming into the cell so more calcium is coming into the cell if more calcium is

coming into the cell we have a lot more calcium rushing in as a lot of calcium rushes in it stimulates again what are

these re receptors here called The ryanodine receptors type two guess what though we have so much calcium in this

sarcoplasmic reticulum now why because the protein k a phosphorated the fosol lamb band to suck a lot of calcium in

there so now also what happened protein K phosphorated these calcium channels the L Type to bring more calcium in as

we bring more calcium in and stimulates the randine receptor type two and now there's so much calcium in the SR that

we release out even more calcium than normal into the piroplasm more calcium means more

interactions with the troponin which moves the tropomyosin if you move the tropomyosin you're going to have more

actin mein interactions what is that called you're going to have significantly increased crossbridge

formations if you have more crossbridge formations you have more power strokes more sliding of the myofilaments so

that's going to increase the actual contractions if it increases the speed of the contractions increases the the

rate of the crossbridge cycling it's going to increase the actual pumping action of the heart and what is this

going to do we'll talk about it more in cardiac output because you know that whenever you

increase the pumping action of the heart the contractility of the heart it increases what's called your stroke

volume and then as a result it can increase your cardiac output and this as a result can increase your blood

pressure okay so that is how the sympathetic nervous system can affect the

contractility because if it affects contractility it's going to increase the actual cycling of the crossbridge

formations it's going to have more contraction speed more heart pumping activity increase in the stroke volume

which is the volume of blood pumped out of The ventricle in one heartbeat and then it's going to increase the amount

of volume of blood that's being pumped out of the ventricles in one minute and that's going to increase your blood

pressure okay so sympathetic nervous system can not only speed up the contractility but increase your blood

pressure at the same time it also increases the heart rate what's the relationship of the heart rate with

blood pressure it's directly proportional remember we said that if you remember here we said cardiac

output is equal to heart rate times stroke volume if you increase the heart rate you increase the cardiac output and

then we said that the cardiac output we actually can rearrange this a little bit better blood pressure is equal to

cardiac output times total peripheral resistance if I increase the cardiac output I increase the blood pressure so

it's a beautiful thing and then same thing with the actual acetylcholine acetylcholine is asking on

the M acting on The muscarinic receptors decreasing the heart rate if you decrease the heart rate you decrease the

cardiac output if you decrease the cardiac output you decrease the blood pressure so these are the beautiful ways

in which your sympathetic nervous system and parasympathetic nervous system can affect the actual nodal and contractile

cells but again parasympathetic only on the nodal cells sympathetic nodal and contractile okay last thing that I want

to talk about here is I want you to see graphically how this this is represented so let me show you here for a second

let's say that I bring here in the graph I bring in let's do it like this I'm going to represent black as

normal for the heart rate here so let's say here's my heart rate I'm up coming up here coming down coming up coming

down right and then same thing here just say this is the normal pacing of the heart rate okay this is what's going to

look like on the graph depolarization repolarization depolarization repolarization you get it but then let's

compare that with the sympathetic nervous system and let's do that in this brown color now the only thing that's

going to be different is is we're going to have action potentials much sooner and it's going to repolarize pretty

quick and it's going to have action potential sooner repolarize quickly and then it's going to repolarize quickly

and then action potential sooner what is the whole point here we're going to have the depolarization occurring much faster

and repolarization is still going to be obeyed we're still going to obey the refractory period but you're going to

notice there's way more frequent Action potentials here that is the effect of the sympathetic nervous system now let's

compare that with another example and let's do this one in green and let's see that the green is the parasympathetic

this time it's going to be a very slow depolarization so it's going to take a longer time to depolarize as it takes a

longer time to depolarize what's happening the rate at which this heart rate is occurring is a lot slower so the

parasympathetic nervous system is going to decrease the action potentials that's the whole purpose sympathetic nervous

system increases the rate of action potentials parasympathetic itic nervous system decreases the rate of action

potentials and that's how this affects the heart rate okay so that covers that last thing

I want to talk about is this whole refractory period because it is important that I briefly mention this

real quick is that this Plateau phase that we talked about here in phase two this Plateau

phase this is important because it's about 250 milliseconds once it comes from this it

starts going into from three all the way to four until there's another action potential this period here is called the

refractory period so this is called the refractory period it's actually broken up into three different parts like you

can have the absolute refractory period the relative refractory period and then another one called a supern normal

refractory period we're not going to talk about that I just want you to understand the refractory period is when

the heart is resting and it's almost about 250 milliseconds too so because of that the refractory period is the time

where the heart is resting this is crucial you want the heart to rest in certain weird

situations as this is going down phase three as it's going down it's getting ready to go into phase four if you

stimulate the heart enough with very very frequent very powerful stimulus you can take it out of refraction and

Trigger another action potential that's called the relative refractory period so there is a weird one here called the

relative refractory period And this is a situation in which you provide enough stimulus to the heart you can take it

out of a fraction and cause another action potential but you don't want to you want to obey the absolute refractory

period it's not as much like a skeletal muscle okay because if you don't it can lead to problems like tetany which can

become very very dangerous if you have Titanic contractions it can very very dangerous so again we want to obey the

absolute refractory period Ninja nerds I can't thank you enough if you guys watch part one you guys watch part two I

guarantee you're really going to know this stuff now and I really hope that it helped I really hope that you guys did

enjoy it if you guys did please please hit the like button comment down in the comment section share the video and

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