Cardiovascular | Electrophysiology | Extrinsic Cardiac Conduction System

Summary

In 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

00:00

💓 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.

05:02

😌 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.

10:03

🏋️‍♂️ 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.

15:04

📈 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.

20:05

👋 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.

Keywords

💡Electrophysiology

Electrophysiology is the study of the electrical properties and activities of biological cells, particularly in the field of medicine. In the context of the video, electrophysiology is used to understand how the heart generates and conducts electrical signals that trigger heartbeats. The script discusses how these signals are regulated by the body to control heart rate and contractility.

💡Extrinsic Regulation

Extrinsic Regulation refers to the external factors that influence a biological system. In the video, it is used to describe how the autonomic nervous system, specifically the sympathetic and parasympathetic nervous systems, regulates the heart rate and contractility of the heart from outside the heart itself.

💡Sympathetic Nervous System

The Sympathetic Nervous System (SNS) is a part of the autonomic nervous system that prepares the body for action, often referred to as the 'fight or flight' response. In the script, the SNS is described as increasing heart rate and contractility, which helps to boost the heart's performance during times of stress or physical activity.

💡Parasympathetic Nervous System

The Parasympathetic Nervous System (PNS) is another branch of the autonomic nervous system that conserves energy and promotes relaxation. The script explains how the PNS works to decrease heart rate and contractility, which is essential for rest and digestion.

💡Beta-1 Adrenergic Receptor

Beta-1 Adrenergic Receptors are specific protein receptors found in the heart that, when activated, increase heart rate and contractility. The script describes how chemicals like norepinephrine and epinephrine bind to these receptors to stimulate the heart, leading to conditions like tachycardia when the heart rate exceeds 100 beats per minute.

💡Tachycardia

Tachycardia is a medical condition characterized by a heart rate greater than 100 beats per minute. The video script uses this term to illustrate the effect of the sympathetic nervous system on the heart, where increased stimulation leads to a faster heart rate.

💡Bradycardia

Bradycardia is a heart rate slower than 60 beats per minute. The script explains that this condition can be induced by the parasympathetic nervous system to slow down the heart rate during rest, promoting relaxation and conservation of energy.

💡Adenyl Cyclase

Adenyl Cyclase is an enzyme that plays a crucial role in signal transduction, converting ATP into cyclic AMP. In the video script, it is mentioned as part of the intracellular process activated by the binding of norepinephrine and epinephrine to the beta-1 adrenergic receptor, leading to increased heart rate.

💡Protein Kinase A

Protein Kinase A (PKA) is an enzyme that transfers a phosphate group from ATP to a protein substrate, thereby regulating its activity. The script discusses how cyclic AMP activates PKA, which then phosphorylates proteins to increase the influx of calcium into heart cells, leading to increased contractility.

💡L-Type Calcium Channels

L-Type Calcium Channels are voltage-gated calcium channels that play a critical role in the heart's electrical activity. The script explains how Protein Kinase A phosphorylates these channels, increasing calcium influx into the cell, which in turn increases the frequency of action potentials and heart rate.

💡Refractory Period

The Refractory Period is a brief period during which the heart muscle cannot respond to electrical signals after depolarization. The script mentions this period to explain the limits of how fast the heart can beat, emphasizing the importance of this resting phase for the heart's health.

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

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always until next time