Full transcript
0:07all right engineers in this video we are
0:09going to talk about
0:10electrophysiology this is an extremely
0:12important topic and the reason why is
0:15because the heart is so special it has
0:17the ability to intrinsically depolarize
0:20itself it doesn't really depend upon the
0:23nervous system we'll talk about how the
0:25nervous system like the extrinsic
0:26inovation of the heart can speed up the
0:29heart rate or decrease the heart rate as
0:31well as maybe even increase the
0:33contractility of the heart we'll discuss
0:34these things but again I want you to
0:36understand something about the heart the
0:37heart exhibits what's called
0:38automaticity what is automaticity so the
0:41heart exhibits a a very important
0:43characteristic and this very very
0:45important characteristic is called
0:49automaticity what is automaticity
0:52automaticity is basically the heart has
0:54its the intrinsic ability on its own to
0:58spontaneously deep polarize itself and
1:02then Trigger action potentials to send
1:04it out to all the other parts of the
1:06heart that is automaticity so one more
1:08time automaticity is the intrinsic
1:10ability of the heart to spontaneously
1:12depolarize and Trigger action potentials
1:15that are spread out all the entire
1:17myocardium the muscle layer of the heart
1:19to trigger the heart muscle to contract
1:22okay that is its intrinsic ability how
1:24does this happen let's get started on
1:26that so what I'm doing is I'm zooming in
1:30here on some cells so before we get into
1:32all that Nitty Gritty components of the
1:34cells I want to take a look at the
1:36larger kind of like gross structure of
1:38this so let's come over here to this big
1:39old heart so in the heart you're going
1:42to have two different types of
1:44components of The myocardium so when you
1:45look at The
1:46myocardium you have two parts so when
1:49you look at The myocardium it's actually
1:51broken up into two components one is
1:55it's broken into what's called nodal
1:58cells which are basically your
2:00non-contract house these are the ones
2:02that generate automaticity these are the
2:04ones that can spontaneously depolarize
2:06generate Action potentials so they don't
2:09contract these for to name a few is
2:11going to be like the SA node which
2:14stands for sinoatrial node AV node which
2:17stands for atrio ventricular node the AV
2:21bundle which is the atrio ventricular
2:23bundle sometimes you might even hear it
2:25referred to as the bundle of
2:28His and there's also going to be What's
2:31called the bundle branches and you have
2:33one bundle branch going to the right
2:35side of the heart one bundle branch
2:36going to the left side of the heart so
2:37for your bundle branches you have both a
2:41left and a right and you have these very
2:44specialized structures that are digging
2:46into very very small components of The
2:48myocardium and these are called your
2:50preni
2:51fibers so again with The myocardium
2:54there's two types of tissue one is these
2:58nodal cells and the noal cells are
3:00non-contractile cells they're the ones
3:02that can intrinsically depolarize
3:04generate action potentials and Trigger
3:05the contraction of the heart these are
3:08SA node AV node AV bundle or bundle of
3:10hiss right and left bundle branches and
3:12your peni fibers the other component of
3:15The myocardium is the contractile cells
3:18so these are the ones that consist of
3:20the actual contractile proteins these
3:23are the ones that consist of actin and
3:27mein and they consist of uh the you know
3:30the troponin and the tropomyosin we
3:33could just keep going on right they
3:34consist of a lot of these contractile
3:36proteins what else they're the one that
3:39actually consist of the sarcoplasmic
3:41reticulum so they consist of that very
3:42specialized structure called the
3:44sarcoplasmic
3:45reticulum so with that said two parts of
3:48The myocardium nodal cells and
3:50contractile cells the ones that are
3:52Contracting they make up the big big
3:54portion of the heart these are the ones
3:56that consist of these contractile
3:57protein units as well as psychop plasmic
3:59ium they're the ones that generate the
4:01force that pushes the blood out of the
4:03heart the nodal cells are the ones that
4:05set a rhythm or a
4:07pace where does this whole pacing or
4:10automaticity start and where can you
4:11find all these structures within the
4:13heart well you got to look right at the
4:15actual pacemaker of this actual
4:18cardiovascular system now that we know
4:19that the myocardium is made up of two
4:21different types of cells nodal cells and
4:22contractile cells we want to focus on
4:24these guys first these nodal
4:26cells where can you find these bad boys
4:29well we got to look at at the pacemaker
4:30we got to look at the one who's actually
4:31generating the heart rhythms or the
4:33sinus rhythm that's this guy he's
4:35actually located right here so what do
4:37we call this guy here he is called the
4:38SA node This Guy's super important where
4:43would you actually find him you're going
4:44to find him if we look here at the
4:45orientation of the heart this is your
4:47right atrium right this is the right
4:49ventricle this is the left ventricle and
4:51this is the left atrium so if you look
4:53into the right atrium right here you're
4:55going to find in the superior component
4:57of the right atrium just beneath this
4:59large vessel here called The Superior
5:01vnea you're going to find this
5:04crescent-shaped structure consisting of
5:06nodal cells that is called the SA node
5:08the SA node is the pacemaker he sets
5:10What's called the sinus rhythm now sinus
5:13rhythm for the SA node is generally he
5:15sets the pace at around 60 to about 80
5:19uh beats per minute now that's really
5:22important because when we have this type
5:24of pace that's the normal heart's
5:27ability so the heart can generate about
5:2960 to 80 beats per minute on its own
5:31without any extrinsic inovation okay
5:33without any autonomic nervous syis so no
5:35sympathetic effect no parasympathetic
5:37effect this is what it can generate on
5:39its own so this normal Pace that we're
5:42setting here around 60 to 80 beats per
5:43minute this is called your sinus rhythm
5:46okay so it's called your sinus
5:51rhythm okay that's your sinus rhythm so
5:54sinus rhythm is generated by the SA node
5:56where it's generating Action potentials
5:59right about 60 to 880 to trigger this
6:02actual heart to beat 60 80 times per one
6:05minute okay that's the normal Sous
6:07Rhythm now we're going to talk about how
6:09it generates Action potentials but
6:11before we do that we need to see where
6:12these Action potentials are getting sent
6:13to we need to know the normal conduction
6:15pathway so this guy is the one that's
6:18generally setting the pace when he sets
6:20this pace he sends this information from
6:23the right atrium into the left atrium
6:25how does he do that you know there's a
6:26specialized structure over here that's
6:29connecting the essay note over here to
6:31the left atrium kind of like a little
6:33special structure over here kind of
6:35spreads out like this it's coming from
6:37over here this right here is called the
6:39Bachman's bundle okay it's called
6:41Bachman's
6:43bundle so this is called
6:46Bachman's bundle and what happens is is
6:50these electrical potentials that Theo
6:52generates he can send some of these
6:54electrical potentials over here through
6:57Bachman's bundle to activate depolarize
7:00the Atria so Isn't that cool so you can
7:02send action potentials from the sa no
7:04which is in the right atrium over to
7:06depolarize the left atrium via Bachman's
7:09bundle another
7:11thing is we have to connect this SA node
7:13here to other parts of the Atria so we
7:16have to connect to other parts of the
7:17Atria so there's other parts here that
7:19can come and Supply different parts of
7:22the Atria here like this what is these
7:26guys here this is actually called the
7:28internodal pathway so all of these guys
7:31here will come out and stimulate
7:32different parts of the Atria and
7:33eventually converge onto that big
7:35structure right there but again what are
7:38all of these fibers right here that are
7:40coming from the essay node outward to
7:42all the other parts of the left atrium
7:43all of these fibers here like this one
7:45and this one and this one these are
7:48making up what's called your
7:51inter
7:54nodal
7:56pathway so saay note to Bachman's bundle
7:58is going from the right atrium to the
8:00left atrium to supply the left atrial
8:02myocardium from the SA node to these
8:04internodal Pathways this will supply all
8:06the other parts of the right atrium but
8:09eventually all of this internodal
8:11pathway will converge onto this second
8:13important structure what is the second
8:15important structure called this second
8:18important structure is called the AV
8:20node okay it's called The Av node the AV
8:25node is so important because look what
8:27he's doing so he's kind of peing
8:30underneath this actual uh pulmonary
8:33trunk here it's actually running from
8:35the actual right atrium and into the
8:37actual this whole thing right here what
8:38is this big structure right here if you
8:40guys watched the video on the structures
8:41and layers of the heart you know that
8:42this would be the interventricular
8:43septum right so that's the
8:45interventricular septum what happens is
8:47this bundle here this AV node runs from
8:51the actual right atrium into the
8:53interventricular septum so it's acting
8:55as a connection the Gateway between the
8:58Atria and the ventricles because what
9:02happens is some of these potentials from
9:03the Bachman's bundle can actually make
9:06their way over here to the AV node also
9:09so some of the action potentials from
9:10the Bachman's bundle can make their way
9:13over here to the AV node so either way
9:15all of the action potentials that are
9:16coming from the SA node that are being
9:18spread out for the interal pathway or
9:19the Bachman's bundle are converging onto
9:21the AV node once the AV node receives
9:24these
9:25signals it's going to take a little bit
9:28of time how long it the actual action
9:32potentials here take about 0.1 second
9:35about 0.1 seconds which is a little bit
9:38longer than how much it takes for them
9:39to move through the SA node cells the
9:41Bachman bundle cells the internodal
9:43pathway cells so because it takes a long
9:46time what's the significance of this
9:47because it has
9:48significance one of the significance
9:51allowing for the AV node to take a 0.
9:53one second delay before it sends the
9:55action potentials down through the
9:56interventricular septum to the bundle of
9:58hiss is because it wants to give
10:02time for Atria to
10:06contract
10:10before the ventricles
10:12contract I can't express how important
10:15this is because of this 0.1 second
10:19delay it gives the time enough adequate
10:22time for the Atria to contract and push
10:24their blood into the left ventricle
10:26because if the AV no were to fire not
10:28have that1 second delay it would it' be
10:29depolarizing The myocardium while the
10:32left atrium and right atrium are trying
10:33to empty their blood into the ventricles
10:35if that's the case then as the
10:36ventricles are getting depolarized they
10:38might start Contracting at the same time
10:40that the Atri are Contracting that's
10:41counterintuitive we don't want that we
10:43want to allow for this guy to contract
10:44squeeze all the blood into the
10:45ventricles then let the ventricles
10:47attain the blood and then squeeze the
10:49vent squeeze the ventricles to push it
10:50out through the aorta and the pulmonary
10:52circulation okay now question is why
10:56does it take 01 second we know that it's
10:58the purpose it gives the time for the
11:00Atria to contract before the ventricles
11:01contract but there's two microscopic
11:04reasons
11:05why these nodal cells are riddled with a
11:08ton of Gap Junctions which are just
11:10basically channels that allow for ions
11:12to pass from cell to cell however the AV
11:16node which consists of a bundle of those
11:17nodal cells it has a lot fewer Gap
11:21Junctions than these other nodal cells
11:24so a lot less Gap Junctions so a lot
11:26less ions can flow from cell to cell
11:28that decreases the ual speed at which
11:30it's moving that's one reason that's why
11:31it takes a little bit longer another one
11:34is because they have a smaller diameter
11:37so the actual fibers are actually a lot
11:41smaller in diameter and if you know a
11:43little bit about conduction we know that
11:45the larger the diameter of the structure
11:47the faster the velocity of that
11:49conduction is going to move so the
11:50smaller the diameter the slower the
11:52conduction speed okay so again we went
11:55from SA node which was the first one
11:57through the Bachman's bundle internodal
11:58pathway into the AV node AV node was the
12:00second one took 01 second delay to give
12:02the time for the Atria to contract empty
12:04their Chambers so that the ventricles
12:06can attain the blood and then they can
12:08contract why does it take the 0.1 second
12:10delay because the AV node has less Gap
12:12Junctions and it has fewer D smaller
12:15diameter muscle fibers okay then where
12:18does it go from here it goes into the
12:21next structure here this next structure
12:24here is going to be kind of like a nice
12:27bundle it's consisting of a big old
12:29bundle right here this guy right there
12:32is called the bundle of hiss okay so
12:35this guy right here is called the bundle
12:37of His or the AV
12:39bundle when he receives these Action
12:41potentials from The Av node he then
12:43conducts it into these two bundle
12:46branches this bundle branch right here
12:49we're going to put here four is going to
12:51the right myocardium so this is the
12:53right bundle branch so which one would
12:55this one be right bundle branch over
12:58here this is going to the left
13:00myocardium so because this is going to
13:02the left myocardium what we say this one
13:03is this is the left bundle branch
13:07because it's going to left myocardium
13:09then from there it goes into these nice
13:11little breaking units you see how this
13:13is branching off branching off branching
13:15off branching off these bundle branches
13:17these are called your preni fibers okay
13:20so these are your preni
13:24fibers okay these are your peni
13:27fibers all right so let's go ahead and
13:29recap these let's recap them in order
13:31now I'm about to get a little taller
13:32okay don't you dare laugh at me I'm
13:34short all right so let's go ahead and
13:36recap the flow so how does it go we said
13:38first things first started at the SA
13:41node he's the pacemaker of the
13:44respiratory I'm sorry the pacemaker of
13:45the actual cardio Cardiovascular Center
13:47right specifically for this actual Pace
13:49setting of the heart rate then what
13:52happens he goes to the next one how does
13:54he get to this next one he goes to the
13:56AV node how does it get to the AV node
13:58remember it travel within the actual
14:00right atrium via the internal pathway
14:02but then the SA node can transmit
14:03impulses to the left atrium via the
14:05Bachman's bundle eventually all of those
14:07fibers converge onto the AV node though
14:10the AV node we said takes about a 0.1
14:13second delay because of the fewer
14:14diameter uh fibers and less Gap
14:17Junctions and to allow for the Atria to
14:19contract and then the ventricles to
14:20contract then from The Av bundle we go
14:23to the bundle of His or again you can
14:26call it the AV bundle doesn't matter
14:29from there it goes into the right and
14:31left bundle branches okay so we're just
14:34going to combine these you can go into
14:35the right and left bundle branches if
14:38it's the right one it's going to the
14:39right myocardium if it's the left bundle
14:40branch it's going to the left myocardium
14:42then from here you're going to go into
14:44the last one which is going to be the
14:46pereni system so the pereni fibers and
14:49this will supply different components
14:52within The myocardium and Trigger The
14:54myocardium to contract we did that now
14:58so now we've covered the actual cardiac
15:01conduction
15:02system okay
15:03sweet from there now what are we going
15:06to do we now now we know the cardiac
15:08induction system the actual gross
15:09anatomy like flow but now we got to be
15:11even more specific how does it generate
15:13these Action potentials how does it
15:15actually do it so now what we're going
15:16to do is we're going to do two things
15:18I'm going to take this sa noal cell I'm
15:21going to take out out of this sa no I'm
15:22going to take and expand on one of the
15:24cells then I'm going to take a piece out
15:28of the myocard and I'm going to expand
15:29that and look at one cell so we're going
15:30to look at two different types of cells
15:32we're going to look at a nodal cell and
15:34we're going to look at a contractile
15:36cell and see how these cells are
15:37communicating and what's all these ion
15:39channels and stuff okay so let's go and
15:41get
15:41started so this cell right here let's
15:44actually just toote it right away this
15:46is our nodal cell okay this is going to
15:48be the nodal cell and this one over here
15:51just so we can get right out of the way
15:53this is going to be the contractile
15:55cell now what did I tell you right away
15:59about the Cellular
16:01Connections we said these two cells okay
16:04because not only are nodal cells because
16:05look I could actually kind of make a
16:06tiny little mini diagram here I can say
16:08that if I have this nodal cell here this
16:10nodal cell could be connected to many
16:12other nodal cells and how could they be
16:15connected what are these little things
16:16that are connecting the nodal cells the
16:18actual Gap Junctions and so if I have
16:21Gap Junctions here this can allow for
16:23ions to pass from this cell to this cell
16:25to this cell to this cell right it's
16:27basically allowing for ions to pass from
16:28cell to to cell the same thing happens
16:31and exists between let's say that this
16:32is a nodal cell and just to make it very
16:34simple I changed the color of the actual
16:36contractile cell I make the contractile
16:38cell black these also have connections
16:42so if these have connections we can
16:43actually allow for ions to flow from a
16:45noal cell into a contractile cell and
16:48then help the contractile cell to start
16:50depolarizing so we're going to see how
16:52that happens but but first before we do
16:54that we got to see how does this guy
16:55depolarize
16:57itself so you know something funny
17:00within these noal cells very funny very
17:02very interesting little cells and they
17:04actually consist of what's called funny
17:07Sony sodium channels you think I'm being
17:09funny but I'm not there's actually funny
17:11sodium channels these channels that are
17:15within this nodal cell are very leaky
17:17and they allow for a little bit of
17:20sodium to leak into the cell very very
17:24slowly very very very slow flow of this
17:27sodium into this noal cell now generally
17:31nodal cells don't have a stable resting
17:33membrane potential normally resting
17:35membrane potential is like -70 toga 90
17:37MTS it depends upon the cell but these
17:40nodal cells don't really have a stable
17:41resting membran potential so their kind
17:43of membrane potential fluctuates but in
17:46general before these sodium channels uh
17:48these funny sodium channels open they
17:51generally are going to have a membrane
17:52potential
17:54around -60 molts that's approximately
17:57where it's at
17:59so now look what happens here let's
18:01let's represent these funny sodium
18:02Channels with
18:03blue these funny funny sodium channels
18:06start actually causing the inside of the
18:07cell to become a little bit more
18:10positive because we're bringing positive
18:11ions into the cell sodium as the sodium
18:15starts coming into the cell something
18:16else really weird starts happening as
18:18you approach the threshold potential
18:20sodium gets a little bit of help okay so
18:22first things first was the sodium is
18:24coming into the cell bringing some
18:26positive charges with it all right this
18:29happens around 60 molts but then what
18:31happens is these other channels they're
18:34called
18:37ttype calcium
18:40channels these are called t types
18:42calcium channels these calcium channels
18:44open
18:45up approximately around - 55
18:50molts so these positive ions are
18:52bringing it from -60 Mill volts to what
18:5655 because it's a really slow flow of
18:58sodium
18:59as it starts flowing in this 55 molts
19:02becomes a stimulus for these ttype
19:06calcium channels when they stimulate
19:08these ttype calcium channels start
19:09opening and calcium starts flowing in
19:11nice and slowly also so now we have the
19:13combined effect of these funny sodium
19:14channels what are these guys here called
19:18funny sodium
19:21channels these are your funny sodium
19:23channels these guys are slowly allowing
19:26for the sodium minus to trickle in then
19:28what happens happens is it stimulates
19:29these ttype calcium channels to come in
19:31once they reach about 55 as these
19:33calcium ions start accumulating with the
19:35sodium ions guess what happens to the
19:36membrane potential it becomes even more
19:38positive let's show that down here so
19:40now if you look you're going to notice
19:43that this is going to be representing
19:44the calcium channels and the sodium
19:46channels look oh shoot they hit
19:49threshold potential what is our
19:51threshold potential here generally
19:53within the cell the threshold these
19:54actual nodal cells is around -40 Ms
19:57normally it's like 50 five in most cells
19:59but in this one it's about
20:01--4 once we hit that -40 another type of
20:05Channel opens up when this channel opens
20:07up it blasts open a lot of calcium and
20:12you're going to see what happens here
20:13that this guy actually Rises pretty
20:15quickly here it rises up very very
20:19quickly and we'll see what happens here
20:21in just a second okay so for right now I
20:23want you to know that whenever we're
20:24inside the cell 60 Ms funny sodium
20:26channels open then around 55 these uh
20:29ttype calcium channels open then when we
20:31hit threshold what channels open these
20:34green channels what are these green
20:35channels here called these green
20:37channels are called L
20:39Type calcium
20:42channels so these are called your L Type
20:45calcium channels they're very very
20:46sensitive to voltage so once this
20:48happens it gets to around -40 Mill volts
20:50and guess who starts flowing in very
20:53powerfully calcium starts flowing in
20:55very very powerfully as the calcium
20:58starts flowing in in very very
20:59aggressively what would you expect to
21:01happen to the inside of the cell to
21:03become super super super positive and
21:05that's what happens look it goes up to-4
21:07and W shoots up how high does it go up
21:11to it generally goes up to
21:15approximately in this cell because the
21:17calcium is coming in very very very
21:19aggressively It generally comes in to
21:21approximately around positive 40 molts
21:26so it comes into about positive 40 molts
21:29as these L Type calcium channels open
21:30the calcium starts rushing in you're
21:32bringing a lot of positive ions into the
21:34cell and as you start bringing tons and
21:37tons and tons of positive ions into the
21:39cell what is it going to do to the
21:40inside of the cell it's going to
21:41depolarize the cell so what's the
21:43overall result here well let's actually
21:45kind of follow what happened here if we
21:46look at this in kind of like a nice
21:47little flow diagram here 60 MTS was the
21:51resting membrane potential the funny
21:53channels open and we brought it to 55
21:55mols right this was when we opened up T
21:58type calcium Chann but T calcium then we
22:01got it from that to threshold potential
22:02which is around 40 MTS this opened up L
22:06Type calcium channels then from that we
22:09took in this L Type calcium channels
22:11when they open calcium flooded in so
22:13aggressively that it completely flipped
22:15the membrane from -4 to about posi 40
22:18molts this is when it's
22:21depolarized so the inside of the cell is
22:23depolarized and extremely positively
22:26charged okay
22:29now we've depolarized the cell it didn't
22:31require any nervous system functioning
22:33isn't that beautiful now here's the
22:35thing how in the heck does that affect
22:37this actual contractile cell these
22:40beautiful Gap Junctions so what happens
22:43is is what are we accumulating a lot of
22:45inside of this cell lots and lots of
22:47positive charges lots of cations ions so
22:50as a lot of these cat
22:52ions are being loaded into these uh into
22:56these actual nodal cells what can happen
22:58well guess what these beautiful Gap
23:01Junctions are connecting they're acting
23:04as the communication Gateway between the
23:06nodal cells and other nodal cells or the
23:08nodal cells and contractile cells so
23:11what do these Gap Junctions actually
23:13made up you know they're made up of
23:13what's called proteins uh specifically
23:16called conin so they're called conin
23:19proteins so there basically a whole
23:21bunch of different types of
23:23conin now these cat I they actually move
23:28through these Gap Junctions into the
23:30other cells they can go from cell to
23:32cell to cell to cell to cell now because
23:36of that I'm bringing positive ions over
23:39into this cell through the Gap Junctions
23:42which is so darn cool but here's the
23:45thing how do we keep these cells so
23:47tightly close together so that the Gap
23:49Junctions aren't separating whenever the
23:51heart's being stretched because we don't
23:53want these actual Gap Junctions to get
23:55separated because it's actually two
23:56different proteins between the cells
23:57connecting together how do I actually
24:00prevent this from happening to keep the
24:01cells so tightly together we have these
24:04special structural proteins here what is
24:06this what is this protein here called
24:09this protein here is called desmosome
24:12okay it's made it has what's called
24:14desmo
24:15zomes now desmosomes are super cool
24:18because they consist of a bunch of
24:19different proteins like for example
24:21these green proteins here that are
24:22connecting the cellto cell lying for the
24:24cellto cell communication these are
24:25called
24:27cadherin and then these proteins here
24:29these blue proteins these are actually
24:31your your attachment plaques and there
24:33could be many different proteins that
24:34make this up it could be what's called
24:36um desmo
24:39plen there could be what's called uh
24:42other different types of chemicals we're
24:44not going to go into all of these
24:45different types I don't want to do that
24:46but there's many different types of
24:47proteins that are making up these
24:49attachment plaques
24:50okay then there's other proteins which
24:54are consisting of these other types of
24:55filaments here that are consisting of
24:57substances like Artin okay so we know
25:01that these desmosomes are basically
25:03acting as like adhesion molecules from
25:05cell to cell connecting the cells
25:08together keeping them very tightly
25:10connected that's really really important
25:12now that leads to a concept whenever I
25:15have two cells communicating together
25:17and I have a combination of
25:19desmosomes and GAP Junctions they
25:22decided hey let's give it a different
25:23name like always right let's let's let's
25:25give this a name so they said it's
25:28actually right over here they said that
25:31whenever you take Gap
25:34Junctions and you add into the
25:37mix
25:38desmosomes they're like oh you know what
25:40let's call
25:42this
25:44inter
25:47collated
25:49discs so inter collated discs are just
25:52basically a bunch of Gap Junctions and a
25:54bunch of Desmos zones connecting the
25:56actual cardiac cells together that's
25:59it so now again what will be happening
26:01over here a lot of cat ions sodium and
26:04and calcium ions are flowing through
26:06these Gap Junctions into this other cell
26:08this contractile cell how does this help
26:10the contractile cell all right let's
26:13see the cell starts becoming a little
26:15bit more positive right we'll see what
26:17happens whenever this cell relaxes in a
26:19second we'll do the relaxation period
26:20together let's keep going with the
26:22depolarization positive ions come over
26:23into this cell when the positive ions
26:26come over into this contractile cell we
26:28have have to think about what is the
26:29actual resting membrane potential of
26:31this cell this one's a little weird this
26:33one was like -60 we said the resting
26:35membrane potential of this cell is right
26:37around 85 to 90 molts okay so its
26:42resting membrane potential is in between
26:45like 85 to 90 Mill volts okay so right
26:49around that now these positive ions
26:54those positive ions that are leaking
26:55into the cell via the Gap Junctions they
26:58start trying to bring the actual
27:00membrane potential closer towards the
27:03threshold that's what they're trying to
27:05do they're trying to bring this closer
27:06towards threshold that's their
27:09purpose but what happens is along that
27:12way okay what's what's threshold
27:14potential within these cells threshold
27:16potential is approximately right around
27:1870 Mill volts within these cells so you
27:21see how different cells can have
27:22different resting member potentials and
27:24threshold potentials it depends upon the
27:26movement of potassium ions okay and
27:29we'll talk about that when we talk about
27:30resting membrane potential with the nerd
27:32equation but what happens is these ions
27:36these cat that are flowing into the cell
27:38are bringing the resting membrane
27:40potential closer to threshold potential
27:42as it does that we reach threshold and
27:45these specialized voltage gated sodium
27:48channels blast open let me see let me
27:51show you where these guys are so here
27:53are the positive ions what is it doing
27:55and originally the cell is at resting
27:57membrane potential it brings it to about
28:00threshold potential which is around -70
28:03molts this stimulates these voltage G
28:06sodium channels these voltage gated
28:08sodium channels start opening when they
28:11open who starts flowing in sodium and
28:14when sodium Flows In he Flows In very
28:17very fast as the sodium lons start
28:20flowing into the cell the inside of the
28:21cell starts becoming very very positive
28:24so it starts becoming very very
28:27positive as it becomes very positive
28:29this positive charge starts moving
28:32across the actual cell membrane or in
28:34this case what's the cell membrane of a
28:35muscle cell called It's called The ccma
28:38so these positive charges start moving
28:40in like a wave around the actual ccma of
28:44the muscle cell
28:45membrane so look at the graph what are
28:47we going to see we were originally at90
28:50we went to 70 through those Gap
28:52Junctions hit threshold potential and
28:54opened up what channels those voltage
28:56gated sodium channels and Rises
28:59up now it rises up kind of a little bit
29:02you know a little bit slower but um what
29:06happens is it gets to
29:09about positive around positive 10 molts
29:14so it gets to approximately around
29:16postive 10
29:18molts now along the way along the way
29:23throughout this process you're
29:24approaching positive 10 molts some other
29:27channels open up a a little bit and
29:28allow for a little bit of calcium to
29:29start trickling in so along this way
29:33another thing that can happen is if we
29:34look over here these black channels
29:36these black channels are calcium
29:37channels these are your calcium channels
29:40and along the way as the sodium is
29:42starting to approach and start causing
29:44the cell to depolarize some of these
29:47calcium channels start slowly opening
29:48only a little bit of them start slowly
29:50opening and calcium starts coming in too
29:52okay so start calcium starts kind of
29:54slowly trickling in also with the Sodium
29:56and this causes that Rising phase there
29:58there it gets to about positive 10
30:01molts when it gets to positive 10 molts
30:04the sodium channels inactivate okay so
30:07they turn off so now the sodium channels
30:09are closed but what else what other
30:11channels open a little bit a little bit
30:12of calcium channels are open very very
30:14little though not too many but what else
30:17decides to open up at the same time
30:19another channel that decides to open up
30:22at the same
30:24time over here is going to be
30:28pottassium
30:29these potassium channels they like ah
30:32you know what it's the perfect time for
30:34me to open up the cell is super super
30:37depolarized let me go ahead and open up
30:39a little bit because we're at positive
30:4110 mols that can't happen we got to
30:43bring it down a little bit so what
30:45happens is these potassium channels open
30:47up and they allow for pottassium ions to
30:49start coming out now the potassium ions
30:52start coming out a little bit more than
30:53the calcium ions are kind of slowly
30:55slowly trickling in so a lot of
30:57potassium ions are going to go out here
30:58for moment of time as that starts
31:01happening what starts happening to the
31:02inside of the cell it's losing positive
31:04charges it's becoming a little bit more
31:06negative what happens then because the
31:09pottassium leaks out of the cell for a
31:11moment it drops down a little bit weird
31:14right has a little drop and it drops
31:17from about 10
31:19molts to around
31:21zero so because of that because of that
31:24actual sodium ions coming in and a
31:26little bit of calcium trickling in it
31:28brings it up to posit 10 MTS at positive
31:3010 sodium channels close potassium
31:32channels open and potassium starts
31:34slowly leaking out a tiny tiny bit of
31:36calcium is coming in and it causes it to
31:39drop down to
31:41around 0
31:44molts when it hits Z molts the calcium
31:47channels those actual volt those voltage
31:49calcium channels become even a little
31:50bit more active they become even a
31:52little bit more active now so once you
31:54hit about positive
31:55zero I guess there is no such thing as
31:58positive z z is positive no matter what
32:01you hit zero Mill volts that becomes a
32:03very powerful stimulus for these L Type
32:05calcium channels okay so these are your
32:07L Type calcium channels as these hit
32:11positive zero they become a little bit
32:12sensitive and the calcium starts flowing
32:16in very
32:18powerfully okay it starts coming in
32:20these positive ions from the calcium
32:22starts coming into the cell but don't
32:25get that Twisted because guess what else
32:26is leaving out at the same time time
32:28just a little bit with it these
32:30potassium ions are also leaving the cell
32:33so because of that we're having
32:34potassium ions leave the Cell at the
32:37same time cat I calcium ions are coming
32:40into the cell so if you think about it
32:42positive ions are leaving and positive
32:43ions are coming in so really there's no
32:45change in the membrane potential well
32:47that's weird so what would that be then
32:50it's going to kind of plateau for a
32:52little bit and it's going to Plateau
32:54actually for a decent amount of time
32:55about 250 milliseconds that's pretty
32:58long time for a cell okay to be in this
33:00depolarized or plateaued like state so
33:03to get this clear first things first we
33:06have this 90 to70 that's due to those
33:09actual uh c those Gap Junctions bringing
33:12the actual ions in to get us to the
33:13actual threshold to allow for the
33:15voltage G the sodium channels to open up
33:17then after that there's a little drop
33:19that little drop there is do the
33:20potassium channels open and more
33:22potassium leaves out than calcium is
33:23coming in and it causes it to go to
33:25positive Z molts or zero molts once we
33:28hit zero those L Type calcium channels
33:30become a little bit more active open up
33:31and a little bit more calcium than
33:33normals coming in but because positive
33:35ions like calcium is coming in and
33:37positive ions like potassium are going
33:38out okay so it's going to Plateau then
33:41let me get some terms out of the way
33:42here just real
33:44quickly doctors I guess wanted to make
33:46it a little bit more complicated for us
33:47so they added
33:49phases the phases that they actually
33:51ordered in it goes from zero to four so
33:55this depolarization phase where the
33:57sodiums are coming in they call that
33:59phase zero okay so phase zero is where
34:01the sodium ions are coming in very
34:03aggressively through the that
34:04depolarizing current the voltage gated
34:06sodium channels then this little dip
34:08down where the potassium channels open
34:11and the potassium starts leaking out to
34:12bring the membrane potential from
34:14positive 10 to zero mainly potassium
34:16very little calciums are coming in this
34:18is called phase one the plateau phase
34:22which is where the calcium is coming in
34:23because we get it to positive Zer and
34:25pottassium are going out so positive
34:27ions are coming in positive Gs are going
34:28out so it's kind of staying around the
34:30same membrane potential not really
34:31changing much this is phase
34:34two now we're going to stay here at
34:36phase two for a little bit because we
34:38have to see how these actual calciums
34:40are leading to contraction so now look
34:42what happens
34:43here these calcium ions until recently
34:46they kind of came up with a theory of
34:48how these calcium ions are actually
34:49triggering the release of other calcium
34:52it's weird right calcium induced calcium
34:54releas is what they call it so what
34:56happens is these calciums that are
34:58flowing in cuz do you know they can
35:00actually flow in what is this little
35:02invagination trust me it's a word I
35:04know these positive ions these actual
35:07calcium can also flow in through this
35:10area too what is this little
35:11invagination here called that
35:12invagination is called a t tual so from
35:15these invaginations sodiums can flow
35:17into the cells and Trigger the calcium
35:18to be released here also from the actual
35:20T tubules reason why I'm telling you
35:22this is because these calcium mines when
35:24they're coming in they're going to go to
35:26this special area with inside the cell
35:28special organel this organel is called
35:30the sarop
35:32plasmic
35:35reticulum what happens is these calciums
35:38have these special special calcium
35:41sensitive channels okay so I'm going to
35:43zoom in on one of these calciums for a
35:45second calcium comes over here and binds
35:48onto a protein one of the proteins is
35:50called
35:51calmodulin now what happens is calcium
35:54and Cal modulin or just calcium can come
35:56over here and bind on to this receptor
35:59very sensitive receptor to calcium this
36:01receptor is called a
36:04ryanodine receptor type two so I'm just
36:07going to put R yr ryanodine receptor
36:10type two this ryanodine receptor type
36:13two which is very sensitive to calcium
36:14whenever there's increas in calcium
36:15levels this ryanodine receptor opens up
36:18a
36:19channel and when it opens up the channel
36:22guess what starts coming out calcium so
36:26now calcium is going to be really
36:28concentrated inside of the sarcoplasmic
36:30culum very very concentrated through
36:32different mechanisms but it's very very
36:34very concentrated guess what starts
36:36coming out of this area now the calciums
36:38so now a lot of calcium is going to get
36:40released out into this actual
36:43sarcoplasm so what happened just over
36:45they're clear calcium stimulate the
36:46Radine receptor type two it can either
36:48do it directly by itself or it can
36:50combine with calmodulin and bind onto
36:52the area which opens up the Radine
36:54receptor type two which is kind of like
36:55a mechanical receptor opens up this
36:58Channel and allows for calcium ions to
36:59come out in excessively large amounts so
37:02now calcium is going to start being very
37:04high within the cytoplasm what is that
37:06calcium going to do well calcium we're
37:08not going to spend a lot of time because
37:09we already have a video on how muscles
37:11contract if you guys haven't seen it go
37:12watch that okay we have a muscle
37:14contraction playlist right where we go
37:15over all this stuff so what happens is
37:18calcium binds onto a special protein
37:21this protein here is called
37:23troponin now this is the only one I want
37:25to spend a little bit of time on is
37:26actually consisting of of three
37:27components troponin i troponin t
37:29troponin c troponin c is where the
37:32calcium binds troponin T is where the
37:35tropomyosin is binding to the troponin
37:37and troponin I is where the troponin is
37:39bound to actin so quickly here it's
37:42bound to actin it's bound to
37:45tropomyosin or it's bound to calcium so
37:49calcium binds onto the troponin cite
37:52which changes the shape of the troponin
37:54it binds with it pulls on troponin t
37:57troponin T pulls on that tropomyosin
37:59protein this orange protein see this
38:01orange protein right here that's
38:03tropomyosin what is it doing it's
38:05impeding the interaction between this
38:08red guy to that green guy what is that
38:09red guy there called that red guy is
38:11called mein so this red this actual red
38:14guy here is called mein this green guy
38:17here is called
38:18actin what happens is calcium binds on
38:21jonin which changes the shape of the
38:24tropomyosin if it changes the shape of
38:26the tropomyosin what happens happens
38:27then let's actually show tropomyosin
38:29like this now so now tropomyosin is out
38:31of the way it's out of the way it's not
38:33impeding it anymore so same thing over
38:35here if calcium binds over here what's
38:37going to happen it's going to move the
38:38tropomyosin out of the
38:40way when tropomyosin is out of the way
38:43guess what can happen the mein head can
38:45interact with the
38:48actin so calcium coming to this area
38:53increases cross
38:56Bridges cross Bridges between the Act
38:59and the me if that's the case then
39:01you're going to have more what is this
39:03kind of representing here me kind of
39:05showing the lines coming in it's
39:06representing the contraction so more
39:08cross Bridges means more
39:12contraction and then that's going to
39:13help to be able to create that pump to
39:17squeeze the blood okay so increase in
39:19the crossbridge interaction increases
39:21the contraction which is going to cause
39:23the heart
39:24to
39:26pump
39:27action okay another
39:31thing because Gap Junctions are
39:33connecting cell to cell this is really
39:35really really really important that
39:37means that these cells are
39:38interconnected that means that these
39:40cells are basically synchronized that
39:42means that whenever these cells are
39:43receiving signals they're receiving it
39:45pretty much all at the same time very
39:46very quickly very very rapid and fast so
39:48these muscle cells that are Contracting
39:52again I could actually say that this is
39:53one muscle cell but at the same time if
39:55I were to come over here for just a
39:56second let's say that I had over here
39:58here's another muscle cell and the ions
40:00from this one are flowing to this one or
40:02they flow over here to this one all of
40:04these muscle cells are going to be
40:05getting depolarized around the same time
40:08so they synchronize their action to
40:10where they contract as a unit they call
40:11this a functional centium not even going
40:14to attempt to spell that okay you can
40:16try to look that up or something okay
40:17how to spell it but again the whole
40:19purpose is is I want you to understand
40:21is that these actual nodal cells are
40:23extending these Action potentials to All
40:25The myocardium through the these Gap
40:27Junctions so because of that they
40:29contract as a unit or they don't
40:31contract at all so this Contracting as a
40:32unit is actually the action of the
40:34functional
40:35centium holy crap that's a heck of a
40:37word right all right so that's that now
40:40so we've seen that action now let's get
40:43into how we actually get this cell to
40:45rest how do we get this cell to rest
40:48well we were at positive 40 molts
40:49because these voltage calcium channels
40:51these L Type calcium channels are open
40:53when we hit positive 40 they shut
40:56off when they shut off another Channel
40:59starts opening very very very powerfully
41:02this is actually going to be called a
41:04potassium Channel and this potassium
41:06Channel opens and potassium starts
41:08exiting the cell as you start losing ton
41:11and tons and tons of pottassium ions you
41:13lose positive ions what starts happening
41:15to the inside of the cell you start
41:16losing positive ions the cell's going to
41:18start becoming a little bit more
41:19negative and it's going to become
41:21negative and more negative and more
41:23negative and then what starts happening
41:24to the inside of the cell it's starting
41:26to
41:27repolarize so you're going to see this
41:31actual line going down on the graph
41:34you'll see it going down and it'll hit
41:36this point of resting membrane potential
41:39so now whenever the pottassium ions are
41:40coming out of the cell it's bringing the
41:42cell from positive 40 molts to around 60
41:45MTS around the resting membrane
41:46potential but again remember these noal
41:48cells don't really have a stable resting
41:50membrane potential once they get to
41:51about -60 the potassium channels close
41:54and those funny sodium channels start
41:56open opening so around 60 you might
41:58notice again these funny sodium channels
42:00opening and then the T type and then the
42:02L Type and then potassium repolarization
42:04okay so it's the same
42:06thing so because of that less cations
42:09are going to be coming into the cell so
42:10this cell is at its peak point now it's
42:12at that platto phase if this cell is at
42:15the plateau phase where the calcium ions
42:16are coming in and pottassium ions are
42:18going out it gets to a point where the
42:21calcium ion channels start closing so
42:25now what happens is
42:28these L typee calcium channels start
42:31closing as these L Type calcium channels
42:33start closing less calcium ions start
42:34coming in another thing we don't want
42:37our muscles to contract forever we got
42:39to get that calcium out of there because
42:40if calcium is there it's just going to
42:41keep binding toonin and keep moving the
42:43tropomyosin out of the way so that the
42:44cross Bridges can keep moving and
42:46creating power strokes and Contracting
42:47the muscle pumping the heart but
42:49eventually the heart's going to get weak
42:50if that happens all the time we have to
42:52give it time to rest so we got to get
42:54this calcium back into the sarcoplasmic
42:57reticulum and out into the extracellular
42:59environment to replenish the calcium
43:01levels in the outside of the cell and
43:03replenish the calcium levels inside of
43:04the sarcoplasmic reticulum how do we do
43:07that so once this happens there's going
43:10to be these special channels over you
43:11see these black channels here in the
43:13coplas reticulum these black channels on
43:16the sarcoplasmic reticulum are actually
43:18going to
43:19move some of this calcium back in so
43:23some of this calcium is going to get
43:24pumped right back into the sarcoplasmic
43:26culum but calcium is moving against his
43:29concentration gradient because you know
43:31calcium is actually going to be in lower
43:34concentration outside the cell and in
43:37high
43:38concentration inside of the coplas
43:40critic so I'm pumping it against so that
43:43means I have to utilize ATP and usually
43:46whenever you utilize the ATP in this
43:47process you're also pumping a proton out
43:50usually so there's usually going to be
43:51an antiporter likee system where you're
43:53pumping a proton out at the same time
43:55you're pumping calcium ions in and it's
43:57utilizing ATP that's get that's
43:59replenishing the calcium levels how else
44:01can we get calcium back in there another
44:04way that we can get calcium back in here
44:05is these
44:07calcium can actually come over to these
44:09other channels over you see these these
44:10actual red channels here these channels
44:13can actually pump some of the calcium
44:14back in also so get some of that calcium
44:18back in but again we have to have
44:20someone to help him because he's going
44:22against his concentration gradient so we
44:23found someone else and he was like Hey
44:25dude no worries I'll help you out I can
44:27move down my concentration gradient and
44:29his name is sodium and sodium moves down
44:33his concentration gradient out of the
44:34cop plasma culum into the cycop plasm
44:37and this is an example of secondary
44:39active transport so again we got calcium
44:42back into the SR through sodium calcium
44:44exchangers or through the calcium proton
44:46ATP ases cool how do we get it back out
44:49the same channels the exact same channel
44:52so now if I take over here this black
44:55channel it's the same thing thing I'm
44:57going to take some of the calcium and
44:59pump it out into the extracellular
45:01environment so this is the ECF the
45:03extracellular fluid this is the protons
45:05I'm going to pump it in I'm going to
45:07have to utilize ATP okay to do this
45:10process because it's primary active
45:11transport then for this one same thing
45:14I'm moving sodium down his concentration
45:18gradient and I'm moving the calcium
45:21against his concentration gradient onto
45:22the ECF that's replenishing the calcium
45:25levels back out here okay say trying to
45:27get your calcium levels out here
45:29replenished and the calcium levels in
45:30the SR
45:31replenished so now that's going to
45:33prevent the contraction so now once that
45:36happens these calcium channels shut off
45:38calcium gets sucked back into the SR
45:39pushed out into the extracellular
45:41environment potassium channels are the
45:42primary ones that are going to be
45:43functioning now functioning now so
45:47pottassium channels are going to even
45:49open up even more and they're going to
45:50start aggressively moving out even more
45:52so as the potassium channels start even
45:54aggressively moving out even more
45:57again you're going to start losing more
45:59and more and more positive ions with no
46:01counteracting of the calcium so what do
46:03you expect if calcium is not
46:05counteracting this anymore what's going
46:06to happen it's going to start dropping
46:09and it's going to drop and it's going to
46:10drop until it gets the resting membrane
46:11potential and then when it drops at the
46:13resting membrane
46:14potential it'll have this brief period
46:17in time where it'll actually kind of
46:19stay rested
46:23until ions from this cell let's say noal
46:27cell leak into this myocardial
46:29contractile cell again via the Gap
46:31Junctions and if that happens what
46:32happens it goes back up to threshold
46:35potential so to finish off phase two is
46:38the plateau phase so let's kind of like
46:40cut that off right there phase one is
46:42the drop down from the potassium
46:43channels phase two is the calcium and
46:45the potassium channels phase three is
46:47just the potassium channels and then we
46:49get into this last phase which is called
46:51phase 4 and phase four is where there's
46:54just no sodium no calcium ion movement
46:56and just potassium ions kind of leaking
46:58out very very slowly to keep it at the
47:01stable resting membrane potential until
47:03the sodium ions or other cats from The
47:05Gap Junctions leak into the cell again
47:07and triggered to go to
47:09threshold holy crap okay that's that
47:13now with that said we see exactly how
47:18this muscle is communicating that's the
47:21intrinsic ability all right Niners if
47:22you guys have stuck in there throughout
47:23this entire video here where we talk
47:25about electrophysiology and very great
47:27detail um I want to thank you guys
47:28enough we're going to I can't thank you
47:29guys enough but we're going to go into
47:30part two so we talked about the
47:31intrinsic ability of the heart what I
47:33want to do now is I want to get into a
47:34little bit more of the detail of the
47:35extrinsic interation of the heart how
47:36that can actually uh bring the actual
47:39Baseline of the intrinsic ability of the
47:40heart above the actual like you know
47:44basically increase in the heart rate or
47:45how we can bring it below that actual
47:47basil rate which is going to be decrease
47:49in the heart rate which is called
47:50bradicardia increase in the heart rate
47:51Tac cardia so we'll talk about how the
47:53sympathetic and parasympathetic nervous
47:55system affects this activity so I hope
47:57to see you guys in part two all right
47:58see you soon n nerds