Cardiovascular | Electrophysiology | Extrinsic Cardiac Conduction System
Summary
TLDRIn this educational video, the focus is on electrophysiology, particularly the extrinsic innervation of the heart. The discussion delves into how the sympathetic and parasympathetic nervous systems regulate heart rate. The script explains the role of neurotransmitters like norepinephrine and acetylcholine, their interaction with receptors such as beta-1 adrenergic and muscarinic M2, and the subsequent cellular processes involving G proteins, adenylate cyclase, and protein kinase A. These mechanisms lead to changes in heart rate, with the sympathetic system causing tachycardia (>100 bpm) and the parasympathetic inducing bradycardia (<60 bpm). The video also touches on the impact of these processes on cardiac contractility and output, emphasizing the importance of adhering to the heart's refractory period for safe and effective functioning.
Takeaways
- 😎 The video discusses electrophysiology, focusing on the extrinsic regulation of the heart, including how to increase or decrease heart rate beyond the normal sinus rhythm.
- 🚀 The sympathetic nervous system can increase heart rate by releasing chemicals like norepinephrine and epinephrine, which bind to beta-1 adrenergic receptors on heart cells, activating a series of intracellular processes that lead to increased calcium influx and depolarization.
- 🌿 The parasympathetic nervous system, particularly through the vagus nerve, can decrease heart rate by releasing acetylcholine, which binds to muscarinic receptors (M2), leading to the activation of inhibitory proteins and the opening of potassium channels, thus hyperpolarizing the cell and slowing down action potentials.
- 💓 An increased heart rate above 100 beats per minute is termed tachycardia, which can be a normal response during exercise or due to sympathetic activation.
- 🐢 A decreased heart rate below 60 beats per minute is termed bradycardia, which can occur during rest or relaxation when the parasympathetic nervous system is more active.
- 🔁 The sympathetic nervous system also affects the contractility of the heart by increasing cyclic AMP levels, which activates protein kinase A. This leads to the phosphorylation of proteins, enhancing calcium influx and leading to stronger contractions.
- 📈 The video uses graphical representations to illustrate the differences in heart rate and action potential frequency under normal conditions, sympathetic activation, and parasympathetic activation.
- 🛑 The refractory period, approximately 250 milliseconds, is crucial for the heart's rest and recovery. It's divided into the absolute refractory period, relative refractory period, and supernormal period, with the importance of obeying the absolute refractory period emphasized to prevent dangerous conditions like tetany.
- 🔄 The video script provides a comprehensive overview of how the autonomic nervous system regulates heart rate and contractility, highlighting the balance between the sympathetic's positive chronotropic and inotropic actions and the parasympathetic's negative chronotropic effects.
Q & A
What is the main topic discussed in the video script?
-The main topic discussed in the video script is electrophysiology, specifically focusing on the extrinsic regulation of the heart rate and the effects of the sympathetic and parasympathetic nervous systems on the heart.
What is the role of the sympathetic nervous system in heart rate regulation?
-The sympathetic nervous system increases heart rate by releasing chemicals like norepinephrine and epinephrine, which bind to beta 1 adrenergic receptors on heart cells. This activates intracellular processes that lead to increased calcium influx, faster depolarization, and ultimately a higher frequency of action potentials, resulting in a higher heart rate.
What is the term used to describe a heart rate greater than 100 beats per minute?
-A heart rate greater than 100 beats per minute is referred to as tachycardia.
How does the parasympathetic nervous system affect heart rate?
-The parasympathetic nervous system decreases heart rate by releasing acetylcholine, which binds to muscarinic type 2 receptors (M2 receptors). This activates a G inhibitory protein that leads to the opening of potassium channels, causing potassium to flow out of the cell. The resulting hyperpolarization slows down the rate of depolarization, reducing the frequency of action potentials and thus decreasing the heart rate.
What is the term used to describe a heart rate less than 60 beats per minute?
-A heart rate less than 60 beats per minute is referred to as bradycardia.
How does the sympathetic nervous system increase the contractility of the heart?
-The sympathetic nervous system increases contractility by activating protein kinase A, which phosphorylates proteins such as phospholamban, leading to increased calcium uptake into the sarcoplasmic reticulum. This results in more calcium being available for release during each action potential, enhancing the strength of muscle contractions and increasing the heart's pumping action.
What is the significance of the refractory period in the context of the heart's electrophysiology?
-The refractory period is a critical time during which the heart's cells are unable to generate another action potential, ensuring that the heart has a rest period. It is divided into the absolute refractory period, where no stimulus can trigger an action potential, and the relative refractory period, where a strong enough stimulus could potentially trigger another action potential.
What is the relationship between heart rate and blood pressure as explained in the script?
-The relationship between heart rate and blood pressure is directly proportional. An increase in heart rate leads to an increase in cardiac output, which in turn increases blood pressure, assuming total peripheral resistance remains constant.
How does the video script describe the effect of acetylcholine on the heart?
-The script describes acetylcholine, released by the parasympathetic nervous system, as binding to muscarinic receptors on heart cells, which then leads to the activation of a G inhibitory protein. This results in the opening of potassium channels, causing potassium to leave the cell and hyperpolarizing it, which slows down the heart rate.
What are the two ways the parasympathetic nervous system can decrease heart rate as mentioned in the script?
-The two ways the parasympathetic nervous system can decrease heart rate are by: 1) activating the beta and gamma inhibitory subunits to bind to potassium channels, allowing potassium to flood out of the cell and hyperpolarize it, and 2) activating the alpha inhibitory subunit to bind to adenylate cyclase, inhibiting the conversion of ATP into cyclic AMP, which decreases protein kinase A levels and thus reduces calcium entry and action potential frequency.
Outlines
💓 Intrinsic and Extrinsic Regulation of Heart Rate
This paragraph delves into electrophysiology, focusing on the extrinsic regulation of the heart. It discusses how the sympathetic and parasympathetic nervous systems influence heart rate, either increasing it above the normal sinus rhythm or decreasing it below. The sympathetic nervous system is highlighted through its interaction with beta-1 adrenergic receptors, which, when stimulated by neurotransmitters like norepinephrine and epinephrine, activate a series of intracellular processes. These processes involve G proteins, adenylate cyclase, and protein kinase A, ultimately leading to the opening of L-type calcium channels and an increase in heart rate. The concept of tachycardia, a heart rate greater than 100 beats per minute, is introduced as a result of this sympathetic stimulation.
😌 Parasympathetic Influence on Heart Rate and Bradycardia
The second paragraph explores the role of the parasympathetic nervous system in slowing down the heart rate. It explains how the release of acetylcholine by parasympathetic neurons affects heart rate by binding to muscarinic type 2 (M2) receptors. This binding activates a G inhibitory protein, leading to the opening of potassium channels and the outflow of potassium ions. The subsequent hyperpolarization of the cell membrane slows down the rate of depolarization, reducing the frequency of action potentials and thus the heart rate. The paragraph introduces bradycardia, defined as a heart rate less than 60 beats per minute, as a result of parasympathetic activation. It also touches on the alpha inhibitory unit's role in inhibiting adenylate cyclase, which decreases cyclic AMP levels and, consequently, reduces calcium entry into the cell, contributing to the slowing of the heart rate.
🏋️♂️ Sympathetic System's Impact on Cardiac Contractility
Paragraph three discusses the sympathetic nervous system's effect on the contractile cells of the heart, in addition to its role on the nodal cells. It details how neurotransmitters like norepinephrine and epinephrine bind to beta-1 adrenergic receptors on these cells, leading to the activation of G proteins and adenylate cyclase. This activation results in increased levels of cyclic AMP and protein kinase A, which phosphorylates proteins such as phospholamban and voltage-gated calcium channels. The increased calcium influx and storage in the sarcoplasmic reticulum enhance the release of calcium during contraction, leading to stronger myocardial contractions. This increase in contractility can raise stroke volume and cardiac output, potentially elevating blood pressure. The paragraph emphasizes the sympathetic nervous system's role in positive chronotropic and inotropic actions, which increase heart rate and contractility, respectively.
📈 Graphical Representation and Refractory Period of Heart Rate Regulation
The fourth paragraph provides a graphical representation of how the sympathetic and parasympathetic nervous systems affect heart rate. It contrasts the normal heart rate pattern with the more frequent action potentials induced by the sympathetic system and the slower rate caused by the parasympathetic system. The concept of the refractory period is introduced, explaining its importance in the cardiac cycle and its duration of approximately 250 milliseconds. The paragraph distinguishes between the absolute refractory period, during which the heart must rest, and the relative refractory period, where strong enough stimuli could potentially trigger another action potential. The dangers of not respecting the refractory period, such as tetany, are briefly mentioned, emphasizing the importance of this physiological mechanism in maintaining regular and safe heart function.
👋 Conclusion and Engagement Invitation
The final paragraph serves as a conclusion, thanking viewers for their engagement with the video content. It encourages viewers to like, comment, share, and subscribe, indicating the presenter's desire for viewer interaction and feedback. The paragraph reinforces the educational value of the video, suggesting that viewers who have watched both parts of the series will have a strong understanding of the material covered. It ends with a farewell, maintaining a friendly and inviting tone for future content.
Mindmap
Keywords
💡Electrophysiology
💡Extrinsic Regulation
💡Sympathetic Nervous System
💡Parasympathetic Nervous System
💡Beta-1 Adrenergic Receptor
💡Tachycardia
💡Bradycardia
💡Adenyl Cyclase
💡Protein Kinase A
💡L-Type Calcium Channels
💡Refractory Period
Highlights
Introduction to electrophysiology and the extrinsic innervation of the heart.
Discussion on how to increase heart rate beyond the sinus rhythm.
Exploration of how to decrease heart rate below the sinus rhythm.
Role of the sympathetic and parasympathetic nervous systems in heart rate regulation.
Mechanism by which the sympathetic nervous system increases heart rate through beta 1 adrenergic receptors.
Intracellular processes activated by the binding of norepinephrine and epinephrine to beta 1 adrenergic receptors.
The function of G stimulatory protein and its role in activating adenylate cyclase.
Conversion of ATP into cyclic AMP and its significance in heart rate regulation.
Protein kinase A's role in targeting L-Type calcium channels to increase calcium influx.
The concept of tachycardia and its association with increased heart rate above 100 beats per minute.
Parasympathetic nervous system's action in slowing the heart rate through acetylcholine release.
The M2 muscarinic receptor's function in the parasympathetic regulation of heart rate.
Impact of potassium channel activation on the cell's polarization and heart rate.
Definition and explanation of bradycardia, where heart rate is less than 60 beats per minute.
Alpha inhibitory unit's role in inhibiting adenylate cyclase and its effect on cyclic AMP levels.
Graphical representation of the sympathetic and parasympathetic nervous systems' effects on heart rate.
Importance of the refractory period in heart health and its duration.
Different phases of the refractory period and their implications for heart function.
Summary of the sympathetic and parasympathetic nervous systems' effects on nodal and contractile cells of the heart.
Closing remarks and call to action for viewers to engage with the content.
Transcripts
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
please subscribe all right Engineers as
always until next time
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