Cardiovascular | Electrophysiology | Intrinsic Cardiac Conduction System

iron engineers in this video we are going to talk about electrophysiology this is an extremely important topic and the reason why is because the heart is so special it has the ability to intrinsically depolarize itself it doesn't really depend upon the nervous system we'll talk about how the nervous system like the extrinsic innervation of the heart can speed up the heart rate or decrease the heart rate as well as maybe even increase the contractility of the heart we'll discuss these things but again I want you to understand something about the heart the heart exhibits was called automaticity what is automaticity so the heart exhibits of a very important characteristic and this very very important characteristic is called Auto Municipality automaticity is basically the heart has its the intrinsic ability on its own to spontaneously depolarize itself and then trigger action potentials to send it out to all the other parts of the heart that is automaticity so one more time automaticity is the intrinsic ability of the heart to spontaneously depolarize and trigger action potentials that are spread out all the entire myocardium the muscle layer of the heart to trigger the more heart muscle to contract okay that is its intrinsic ability how does this happen let's get started on that so what I'm doing is I'm zooming in here on some cells so before we begin to all that needy greedy components of the cells I want to take a look at the larger kind of like gross structure of this so it's come over here to this big old heart so in the heart you're going to have two different types of components of the myocardium so when you look at the myocardium you have two parts so when you look at the myocardium it's actually broken up into two components one is it's broken into what's called nodal cells which are basically your non contractile cells these are the ones that generate automaticity these are the ones that can spontaneously depolarize generate action potentials so they don't contract these fer to name a few is going to be like the SA node which stands for sinoatrial node AV node which stands for atrial ventricular node the AV bundle which is the atrioventricular bundle sometimes you might even hear it referred to as the bundle of His and there's also going to be what's called the bundle branches and you have one bundle branch going to the rights of the heart one bundle branch going to the left out of the heart so for your bundle branches you have both a left and a right and you have these very specialized structures that are deep digging into very very small components of the myocardium and these are called your Purkinje fibers so again with the myocardium there's two types of tissue one is these nodal cells and the nodal cells are non contractile cells they're the ones that can intrinsically be polarized generate action potentials and trigger the contraction of the heart these are SA node AV node AV bundle or bundle of his-- right left bundle branches in your Potenza fibers the other component of the myocardium is the contractile cells so these are the ones that consist of the actual contractile proteins these are the ones that consist of actin and myosin and they consist of the you know the troponin and the tropomyosin we could just keep going on right to consists of a lot of these contractile proteins what else they're the one that actually consists of the sarcoplasmic reticulum so they consist of that very specialized structure called the sarcoplasmic reticulum so with that said two parts of the myocardium nodal cells and contractile cells the ones that are contracting they make up the big big portion of the heart these are the ones that consist of these contractile protein units as well as sarcoplasmic reticulum they're the ones that generate the force that pushes the blood out of the heart the nodal cells are the ones that set a rhythm or a pace where does this all pacing automaticity start and where can you find all these structures within the heart we got to look right at the actual pacemaker of this actual cardiovascular system now that we know to my apartment with two different types of cells nodal cells and contractile cells we want to focus on these guys first these know cells where can you find these bad boys we got a look at the pacemaker we got a look at the one who's actually generating the heart rhythms or the sinus rhythm that's this guy he's actually located right here so what do we call this guy here he is called the SA node this guy's super important why would you actually find them you're going to find them if we look here at the orientation of the heart this is your right atrium right this is the right ventricle this is the left ventricle and this is the left atrium so if you look into the right atrium right here you're going to find in the superior component of the right atrium just beneath this large vessel here called the superior vena cava you're going to find this crescent-shaped structure consisting of nodal cells that is called the SA node the SA node is the pacemaker he sets what's called the sinus rhythm now sinus rhythm for the SA node is generally he sets the pace at around 60 to about 80 beats per minute now that's really important because we have this type of pace that's the normal heart's ability so the heart can generate about 60 to 80 beats per minute on its own without any extrinsic innervation okay without any autonomic nervous sono sympathetic effect no parasympathetic effect this is what it can generate on its own so this normal pace that we're setting around 60 to 80 beats per minute this is called your sinus rhythm okay so it's called your sinus rhythm okay that's your sinus rhythm so sinus rhythm is generated by the SA node where it's generating action potentials right about 60 to 80 to trigger this actual heart to beat 60 80 times per one minute okay that's the normal sinus rhythm now we're going to talk about how it generates action potentials before we do that we need to see where these action potentials are getting sent to we need to know the normal conduction pathway so this guy is the one that's generally setting the pace when he sets this pace he sends this information from the right atrium into the left atrium how did he do that you know there's a specialized structure over here that's connecting the SA node over here to the left atrium kind of like a little special structure over here kind of spreads out like this it's coming from over here this right here is called the Bachmann bundle okay it's called Bachmann's bundle so this is called Bachmann's bundle and what happens is is these electrical potentials that the SA node generates he can send some of these electrical potentials over here through Bachmann's bundle to activate and depolarize the atria so it's not cool so you can send action potentials from the SA node which is in the right atrium over to depolarize the left atrium via Bachmann's bundle another thing is we have to connect to this SA node here to other parts of the atria so we have to connect to other parts of these ER so there's other parts here that can come and supply different parts of the atria here like this what is these guys here this is actually called the internodal pathways so all of these guys here will come out and stimulate different parts of the atria and eventually converge onto that big structure right there but again what are all of these fibers right here that are coming from the SA node outward to all the other parts of the left atrium all of these fibers here like this one and this one and this one these are making up what's called your inter nodal pathway so SA node two Bachmann's bundle is going from the right atrium to the left atrium to supply the left atrium of myocardial from the SA node to these internodal pathways this will supply all the other parts of the right atrium but eventually all of this internodal pathways converge onto this second important structure what is the second important structure called this second important structure is called the AV node okay it's called the AV node the AV node is so important because look what he's doing so he's kind of peeking underneath this actual pulmonary trunk here it's actually running from the actual right atrium and into the actual this whole thing right here what is this big structure right here if you guys watch the video on the structures and layers a little heart you know that this would be the interventricular septum all right so that's the interventricular septum what happens is this bundle here this AV node runs from the actual right atrium a to the interventricular septum so it's acting as a connection the gateway between the atria and the ventricles because what happens is some of these potentials from the Bachmann's bundle can actually make their way over here to the AV node also so some of the action potentials from the Bachmann's bundle can make their way over here to the AV node so either way all of the action potentials that are coming from the SA node that are being spread out to the internet'll pathway or the Bachmann's bundle are converging onto the AV node once the AV nodes receives these signals it's going to take a little bit of time how long it the actual action potentials here take about 0.1 second about 0.1 seconds which is a little bit longer than how much it takes for them to move through the SA node cells the Baughman bundle cells the internodal pathways cells so because it takes a long time what's the significance of this because it has significance 1 xored significance allowing for the AV node to take a point 1 second delay before it sends the action potentials down through the interventricular septum to the bundle of hiss is because it wants to give time for atria to contract before the ventricles contract I can't express how important this is because of this point 1 second delay it gives the time enough adequate time for the atria to contract and push their blood into the left ventricle because if the AV node were to fire not have that point 1 second delay it would it be to polarizing the myocardium while the left atrium and right hm I'm trying to empty their blood into the ventricles if that's the case then as the ventricles are going to be polarized they might start contracting at the same time that the atria contracting that's counterintuitive we don't want that we want to allow for this guy to contract squeeze all the blood into the ventricles then let the ventricles obtain the blood and then squeeze the venture squeeze the ventricles to push it out through the aorta and the pulmonary circulation okay now question is why does it take point 1 second we know that it's the purpose it gives the time for the atria to contract before the ventricles contract but there's two microscopic reasons why these nodal cells are riddled with a ton of gap junctions which are just basically the channels that allow for ions to pass from cell to cell however the AV node which consists of a bundle of those nodal cells it has a lot fewer gap junctions than these other nodal cells so a lot less gap junctions so a lot less ions can flow from cell to cell that decreases the actual speed at which it's moving that's one reason that's why I take a little bit longer another one is because they have a smaller diameter so the actual fibers are actually a lot smaller in diameter and if you know a little bit about conduction we know that the larger the diameter of the structure the faster the velocity of the conduction is going to move so the smaller the diameter the slower the conduction speed okay so again we went from SA node which was the first one through the Bachmann's bundle internodal pathway into the AV node AV node was the second one to a point 1 second delay to give the time for the atria to contract empty their chambers so that the ventricles can attain the blood and then they can contract why does it take the point one second delay because the AV node has less gap junctions and it has fewer diet' a smaller diameter muscle fibers okay then where does it go from here it goes into the next structure here this next structure here is going to be kind of like a nice bundle it consists in a big ol bundle right here this guy right there it's called the bundle of hiss okay so this guy right here is called the bundle of His or the AV bundle when he receives these action potentials from the AV node he then conducts it into these two bundle branches this bundle branch right here we're going to put here for is going to the right myocardium so this is the right bundle branch so which one with this one B right bundle branch over here this is going to the left myocardial so because this is going to the left mark are diem what we say this one is this is the left bundle branch because going to the left my accordion then from there it goes into these nice little breaking units you see how this is branching off branching off branching off branching off these bundle branches these are called your Purkinje fibers okay so these are your Purkinje fibers okay these are your four Kinji fibers all right so let's go ahead and recap these let's recap them in order now I'm about to get a little taller okay don't you dare laugh at me I'm short alright let's go ahead and recap the flow so how does it go we said first things first started at the SA node he's the pacemaker of the respiratory I'm sorry the pacemaker of the actual cardiovascular center right specifically for this actual pace setting of the heart rate then what happens he goes to the next one how does he get to this next one he goes to the AV node how does it get to the AV node remember it travels within the actual right atrium via the internal pathway but then the SA node can transmit impulses to the left atrium via the Bachmann's bundle eventually all of those fibers convert onto the AV node though the AV node we said takes about a point one second delay because of the fewer diameter fibers and less gap junctions until after the atria to contract and then the ventricles to contract then from the AV bundle we go to the bundle of his or again you can call it the AV bundle doesn't matter from there it goes into the right and left bundle branches okay so we're just going to combine these you can go into the right and left bundle branches if it's the right one it's going to the right myocardial if it's the left bundle branches going to the left mark our deal then from here you're going to go into the last one which is going to be the Purkinje systems or the Purkinje fibers and this will supply different components within the myocardium and trigger the myocardium to contract we did that now so now we've covered the actual cardiac conduction system okay sweet from there now what are we going to do we now now we know the cardiac conduction system the actual gross anatomy like flow but now we got to be even more specific how does it generate these action potentials how does it actually do it so now we're going to do is we're going to do two things I'm going to take this SA nodal cell I'm going to take out out of this SA node I'm going to take and expand on one of the cells then I'm going to take a piece out of the myocardium and I'm expand that look at one cell so we're going look at two different types of cells we're going to look at a nodal cell and we're going to look at a contractile cell and see how these cells are communicating and what's all these ion channels and stuff okay so it's going to get started so this cell right here let's actually just denote it right away this is our noble cell okay this is going to be the nodal cell and this one over here just we can get right out of way this is going to be the contractile cell now what did I tell you right away about the cellular connections we said these two cells okay because not only our nodal cells because look I could actually kind of make it that tiny little mini diagram here I can say that if I have this nodal cell here this nodal cell could be connected to many other nodal cells and how could they be connected what are these little things that are connecting the nodal cells the actual gap junctions and so if I have gap junctions here this can allow for ions to pass from this cell to this cell to this cell to this cell right it's basically on four ions to pass from cell to cell the same thing happens and exists between let's say that this is a nodal cell and just to make it very simple I change the color of the actual contractile cell I make the contractile cell black these also have connections so if these have connections we can actually allow them for ions to flow from a nodal cell into it a contractile cell and then help the contractile cell to start depolarizing so we're going to see how the habits over first before we do that we got to see how does this guy depolarize itself so you notice something funny within these nodal cells very funny very very interesting little cells and they actually consists of called funny so neat a sodium channel you think I'm being funny but I'm not there's actually funny sodium channels these channels that are within this nodal cell are very leaky and they allow for a little bit of sodium to leak into the cell very very slowly very very very slow flow of this sodium into this nodal cell now generally nodal cells don't have a stable resting membrane potential normally resting membrane potential is like negative 70 to negative 90 millivolts it depends upon the cell but these nodal cells don't really have a stable resting member Angell so they're kind of membrane potential fluctuates but in general before these sodium channels are these funny sodium channels open they generally are going to have a membrane potential around negative 60 millivolts that's approximately where it's at so now look what happens here let's represent these flooding sodium channels with blue these funny employee sodium channels start actually causing the inside of the cell to become a little bit more positive because we're bringing positive ions into the cell sodium as the sodium starts coming into the cell something else really weird starts happening as you approach the threshold potential so do you get a little bit of help okay so first things first was the sodium is coming into the cell bringing some positive charges with it all right this happens around negative 60 millivolts but then what happens is these other channels they're called t-type calcium channels these are called pea types calcium channels these calcium channels open up approximately around negative 55 millivolts so these positive ions are bringing it from negative 60 millivolts to what negative 55 because it's a really slow flow of sodium as it starts flowing in this negative 50 mi 5 millivolts becomes a stimulus for these t-type calcium channels when they stimulate these t-type calcium channels start opening and calcium starts flowing in nice and slowly also so now we have the combined effect of these funny sodium channels what are these guys here called funny sodium channels these are your funny sodium channels these guys are slowly allowing for the sodium ions to trickle in then what happens is it stimulates these t-type calcium channels to come and once they reach about negative 55 as these calcium ions start accumulating with the sodium line guess what happens to the membrane potential it becomes even more positive let's show that down here so now if you look you're going to notice that this is going to be representing the calcium channels and me sodium channels look oh shoot they hit threshold potential what is our threshold potential here generally within the cell the threshold is actual nodal is around negative 40 millivolts normally it's like negative 55 in most cells but this one's about negative 40 once we hit that negative 40 another type of channel opens up when this channel opens up it blasts open a lot of calcium and you're going to see what happens here that this guy actually Rises pretty quickly here it rises up very very quickly and we'll see what happens in just a second okay so for right now I want you to know that whenever we're inside the cell negative 60 millivolts flooding sodium channels open then around negative 55 these t-type calcium channels open do when we hit threshold what channels open these green channels what are these green channels they're called these green channels are called metal type calcium channels so these are called your l-type calcium channels are very very sensitive to voltage so once this happens it gets to run negative 40 millivolts and guess who starts flowing in very powerfully calcium starts flowing in very very powerfully as the calcium starts flowing in very very aggressively what would you expect to happen to the inside of the cell to become super super super positive and that's what happened look it goes up to negative 40 Wow shoots up how high does it go up to it generally goes up to approximately in this cell because the calcium is coming in very very very aggressively it generally comes in to approximately around positive 40 millivolts so it comes in to about positive 40 millivolts as these l-type calcium channels open the calcium starts rushing in you're bringing a lot of positive ions into the cell and as you start bringing tons and tons and tons of positive ions into the cell what is it going to do to the inside of the cell is going to depolarize the cell so what's the overall result here well it's actually kind of follow what happened here if we look at this in kind of like a nice little flow diagram here negative 60 millivolts was the resting membrane potential the funding channels open and we brought it to negative 55 millivolts right this is when we opened up t-type calcium channel fatty calcium then we got it from that to threshold potential which is around negative 40 millivolts this opened up l-type calcium channels then from that we took in this l-type calcium channels when they open calcium flooded in so aggressively that it completely flipped the membrane from negative 40 to about positive 40 millivolts this is when it's be polarized so the inside of the cells depolarize and extremely positively charged okay now we've depolarize the cell it didn't require any nervous system functioning isn't it beautiful now here's the thing how in the heck does that affect this actual contractile cell these beautiful gap junctions so what happens is what are we accumulating a lot of inside of the cell lots and lots of positive charges lots of cations so as a lot of these cations are being loaded into these into these actual nodal cells what can happen well guess what these beautiful gap junctions are connecting they're acting as the communication gateway between the nodal cells and other nodal cells are the nodal cells and contractile cells so what any gap junctions actually made up another made up of what's called proteins specifically called connections so they're called connection proteins so basically a whole bunch of different types of connections now these cations they actually move through these gap junctions into the other cells they can go from cell to cell to cell to cell to cell now because of that I'm bringing positive ions over into this cell through the gap junctions which is so darn cool but here's the thing how do we keep these cells so tightly closed together so that the gap junctions aren't separating whenever the heart's being stretched because we don't want these actual gap junctions to get separated because it's actually two different proteins between the cells connecting together how do I actually prevent this from happening to keep the cells so tightly together we have these special structural proteins here what is this what is this protein here cold this protein here is called desmosomes okay it has what's called desmo zomes now desmosomes are super cool because they gets us up a bunch of different proteins like for example these green proteins here that are connecting the cell-to-cell lying for the cell-to-cell communication these are called cat hearings and then these proteins here these blue proteins these are actually your attachment plaques and there could be many different proteins that make this up it could be what's called a desmo plaque in there could be what's called other different types of chemicals we're not going to go into all of these different types I don't want to do that but there's many different types of proteins that are making up these attachment plaques okay then there's other proteins which are consisting of these other types of filaments here that are consisting of substances like keratin okay so we know that these desmosomes are basically acting is like adhesion molecules from cell to cell connecting themselves together keeping them very tightly connected that's really really important now that leads to a concept whenever I have two cells communicating together and I have a combination of desmosomes and gap junctions they decided hey let's give it a different name like always all right let's give this a name so they said it's actually right over here they said that whenever you take gap junctions and you add into the mix desmosomes they're like I not like to call this inter collated disks so intercalated disks are just basically a bunch of gap junctions and a bunch of desmosomes connecting the actual cardiac cells together that's it so now again will be happening over here a lot of cations sodium and calcium ions are flowing through these gap junctions into this other cell this contractile cell how does this help the contractile cell all right let's see the cell starts becoming a little bit more positive right we'll see what happens whenever this cell relaxes in a second we'll do the relaxation period together let's keep going with the depolarization positive ions come over into this cell when the positive ions come over into this contractile cell we have to think about what is the actual resting membrane potential of this cell this one's a little weird this one was like negative 60 we said the resting membrane potential of this cell is a right around negative 85 to negative 90 millivolts okay so it's resting membrane potential is in between like negative 85 to negative 90 millivolts okay so right around that now these positive ions those positive ions that are leaking into the cell because gap junctions they start trying to bring the actual membrane potential closer towards the threshold that's what they're trying to do trying to bring this closer towards threshold that's the purpose but what happens is along that way okay let's what threshold potential within these cells threshold potential is approximately right around negative 70 millivolts within these cells so you see how different cells can have different resting membrane potentials and threshold potentials it depends upon the movement of potassium ions okay we'll talk about that when we talk about resting membrane potential with the Nernst equation but what happens is these ions these cations that are flowing into the cell are bringing the resting membrane potential closer to threshold potential as it does that we reach threshold any specialized voltage-gated sodium channels blast open let me see let me show you where these guys are so you hear the positive ions what is it doing and originally the cells at resting membrane potential it brings it to about threshold potential which is around negative 70 millivolts this stimulates these voltage-gated sodium channels these voltage-gated sodium channels start opening when they open who starts flowing in sodium and when sodium flows in he flows in very very fast as the sodium ions start flowing into the cell the inside the cell starts becoming very very positive so it starts becoming very very positive as it becomes very positive this positive charge starts moving across the actual cell membrane or in this case what's the cell membrane of the muscle cell called it's called the sarcolemma so these positive charges start moving and like a wave around the actual sarcolemma of the muscle cell membrane so look at the graph what are we going to see we were originally at negative 90 we went to negative 70 through those gap junctions hit threshold potential and opened up what channels those voltage-gated sodium channels and it rises up now it rises up kind of a little bit you know a little bit slower but what happens is it gets to about positive around positive 10 millivolts so it gets to approximately around positive 10 millivolts now along the way along the way throughout this process you're approaching positive 10 millivolts some other channels open up a little bit and allow for a little bit of calcium to start trickling in so along this way another thing that can happen is if we look over here these black channels these black channels are calcium channels these are your calcium channels and along the way as the sodium is starting to approach and start causing the cell to depolarize some of these calcium channels starts slowly opening only a little bit of them starts slowly opening calcium starts coming in - okay so special accustomed starts kind of slowly trickling in also with the sodium and this causes that rising phase there it gets to about positive 10 millivolts when it gets deposited 10 millivolts the sodium channels inactivate okay so they turn off so now the sodium channels are closed but what else what other channels open a little bit a little bit of calcium channels are open very very little but not too many but what else decides to open up at the same time another channel that decides to open up at the same time over here is going to be potassium these potassium channels they like I you know what it's the perfect time for me to open up the cell is super super depolarized let me go ahead and open up a little bit because we're a positive 10 millivolts that can't happen we got to bring it down a little bit so what happened is these potassium channels open up and they allow for potassium lines to start coming out now the potassium ions start coming out a little bit more than the calcium ions are kind of slowly slowly trickling in so a lot of potassium ions are going to go out here from of time as that starts happening one starts happening to the inside of the cell it's losing positive charge it's becoming a little bit more negative what happens in because the potassium leaks out of the cell for a moment it drops down a little bit weird right as a little drop and it drops from about ten millivolts to around zero so because of that because of that actual sodium ions coming in a little bit of calcium trickling in it brings it up to positive ten millivolts at positive ten sodium channels close potassium channels open and potassium starts slowly leaking out a tiny tiny bit of calcium is coming in and it causes it to drop down to around zero millivolts when they hit zero millivolts the calcium channels those actual volt those voltage-gated calcium channels become even a little bit more active to become even a little bit more active now so once you hit about positive zero I guess there is no such thing as positive zero zero is positive no matter one you zero millivolts that becomes a very powerful stimulus for these l-type calcium channels okay so these are your l-type calcium channels as these hit positive zero they become a little bit sensitive and the calcium starts flowing in very powerfully okay it starts coming in these positive ions from the Cata calcium starts coming into the cell but don't get that twisted because guess what else is leaving out at the same time just a little bit with it these potassium ions are also leaving the cell so because of that we're having potassium ions leave this cell at the same time cations calcium ions are coming into the cell so if you think about it positive ions are leaving and positive ions are coming in so really there's no change in the membrane potential that's weird so what would that be then it's going to kind of plateau for a little bit and it's going to plateau actually for a decent map about 250 milliseconds that's pretty little these a long time for a cell okay to be in this deep polarized or plateaued like state so to get this clear first things first we have this negative nine to negative seventy that's due to those actual caddos gap junctions bring in the actual eye to get us to the actual threshold to offer the voltage-gated sodium channels to open up then after that there's a little drop that little drop there's do the potassium channels open and more potassium leaves out than calcium is coming in and it costs it to go to positive zero millivolts are zero millivolts once we have zero those l-type calcium channels become a little bit more active open up and a little bit more calcium than normal is coming in but because positive ions like calcium is coming in and positive ions like potassium are going out so it's going to plateaued it let me get some terms out of the way here just real quickly doctors I guess wanted to make it a little more complicated for us so they added phases the phases that they actually order it in it goes from zero to four so this depolarization phase where the sodium ions are coming in they call that phase zero okay so phase zero is where the sodium ions are coming in very aggressively through that depolarizing current the voltage-gated sodium channels then this little dip down where the potassium channels open and the potassium starts leaking out to bring the membrane potential from positive ten to zero mainly potassium very little calcium ions are coming in this is called phase one the plateau phase which is where the calcium is coming in because we get it to positive zero and potassium are just going out so positive ions are coming in positive ions are going out so it's kind of staying around the state membrane potential not really changing much this is phase two now we're going to stay here at phase two for a little bit because we have to see how this actual calcium ions are leading to contraction so now look what happens here these calcium ions until recently they kind of came up with a theory of how these calcium ions are actually triggering the release of other calcium ions because it's weird right calcium induced cows and releases what they call it so what happens is these calcium ions that are flowing in because you know they can actually flow in what is this little invagination trust me it's a word I know these positive ions these actual calcium ions can also flow in through this area too what is this little imagination you're called that imagination is called a t tubules so from these imagination sodium ions can flow into the cells and trigger the calcium to be released here also from the actual t tubules reason why i'm telling you this is because these calcium ions when they're coming in they're going to go to the special area with inside of the cell special organelle this organelle is called the Sarco plasmic reticulum what happens is these calcium ions have B special special calcium-sensitive channels okay so I'm going to zoom in on one of these calcium for a second calcium comes over here and binds on to a protein one of the proteins is called calmodulin now what happens is calcium and calmodulin or just calcium can come over here and bind on to this receptor very sensitive receptor to calcium this receptor is called a ryanodine receptor type ii so I'm going to put ROI R ryanodine receptor type to this ryanodine receptor type ii which is very sensitive to calcium whenever there's increasing calcium levels this ryanodine receptor opens up a channel and when it opens up the channel guess what starts coming out calcium so now calcium is going to be really concentrated inside of the sarcoplasmic reticulum very very concentrated through different mechanisms but it's very very very concentrated guess what starts coming out of this area now the calcium ions so now a lot of calcium is going to get released out into this actual sarcoplasm so what happened just so they're clear calcium stimuli the ranitidine receptor type 2 it can either do it directly by itself or it can combine with calmodulin and bind onto the area which opens up the r and Adeem receptor type 2 which is kind of like a mechanical receptor opens up this channel and allows for calcium ions to come out in excessively a large amounts so now calcium is going to start being very high within the sarcoplasm what is that calcium going to do with calcium we're not going to send a lot of time because we already have a video on how muscles contract you guys haven't seen it go wash that okay we have a muscle contraction playlist right we go over all this stuff so what happens is calcium binds onto a special protein this protein here is called troponin now this is only one i want to spend a little bit of time on is actually consisting of three components troponin i troponin t troponin c troponin c is where the calcium binds troponin t is where the tropomyosin is binding to the troponin and troponin i is where the troponin is down to actin so quickly here it's not into acting it's behind a tropomyosin or it's bound to calcium so calcium binds onto the troponin C site which changes the shape of the troponin it binds when it pulls in troponin T troponin t2 pulls on that triple myosin protein this orange proteins is orange protein right here that's triple myosin what is it doing it's impeding the interaction between this red guy to that green guy what does that red guy they're called that red guy is called myosin so there's red this actual red guy here is called myosin this green guy here is called actin what happens is calcium binds on such opponent which changes the shape of the tropomyosin if it changes the shape of the tropomyosin what happens then let's actually show triple myosin like this now so not tropomyosin is out of the way because I was away it's not impeding it anymore so same thing over here if calcium binds over here what's going to happen it's going to move the tropomyosin out of the way when tropomyosin is out of the way guess what can happen the myosin head can interact with the actin so calcium coming to this area increases cross bridges cross bridges between the act and the myosin if that's the case then you're going to have more what is this kind of representing here me kind of showing the lines coming in it's representing the contraction so more cross bridges means more contraction and then that's going to help to be able to create that pump to squeeze the blood ok so increasing the cross bridge interaction increases the contraction which is going to cause the heart to pump action ok another thing because gap junctions are connecting cell to cell this is really really really really important that means that these cells are interconnected that means these cells are basically synchronized that means that whenever these cells are receiving signals they're receiving it pretty much all at the same time very very quickly very very rapid and fast so these muscle cells that are contracting again I could actually say that this is one muscle cell but at the same time have already come over here for just a second let's say that oh go ahead over here here's another muscle cell and the ions from this one flow into this one or they flow over here to this one all of these muscle cells are going to be getting depolarized around the same time so they synchronize their action to where they contract as a unit they call this a functional syncytium not even going to attempt to spell that okay you can try to look that up or something okay how to spell it but again the whole purpose is as I want you to understand is that these actual nodal cells are extending these action potentials to all the myocardium through these gap junctions so because of that they contract as a unit or they don't contract at all so this contracting as a unit is actually the action of a functional syncytium holy crap that's a heck of a word right alright so that's that now so we've seen that action now let's get into how we actually get this cell to rest how do we get to self rest we were at positive 40 millivolts because these voltage-gated calcium channels l-type calcium channels are open when we have positive 40 they shut off when they shut off another channel starts opening very very very powerfully this is actually going to be called a potassium channel and this potassium channel opens and potassium starts exiting the cell as you start losing ton in tons and tons of potassium lines you lose positive ions what starts happening to the inside of the cell you start losing positive ions my cells gonna start becoming a little bit more negative and it's going to become negative and more negative and more negative and then one start tapping to the inside of the cell it's starting to repolarize so you're going to see this actual line going down on the graph you'll see it going down it'll hit this point of resting membrane potential so now whenever the potassium ions are coming out of the cell it's bringing this cell from positive 40 millivolts to around negative 60 millivolts around the resting membrane potential but again remember these all cells don't really have a stable resting membrane potential once they get to about negative 60 the potassium channels close and those funny sodium channels start opening so around negative 60 you might notice again these funny sodium channels opening and then the T type and then the L type and then potassium repolarization okay so it's the same thing so because of that less cations are going to be coming into the cell so this cell is at its peak point now it's at that plateau phase if this cells at the plateau phase where the calcium ions are coming in and potassium ions are going out it gets to a point where the calcium ion channels start closing so now what happens is these l-type calcium channels start closing as these l-type calcium channels start closing less calcium ions start coming in another thing we don't want our muscles to contract forever we got to get that calcium out of there because if calcium is there it's just going to keep binding troponin and keep moving the tropomyosin out of the way so that the cross bridges can keep moving and creating power strokes and contracting the muscle pumping heart but eventually the hearts can get weak if that happens all the time we have to give it time to rest so we got to get this calcium back into the sarcoplasmic reticulum and out into the extracellular environment to replenish the calcium levels in the outside of cell and replenish the calcium level inside of the sarcoplasmic reticulum how do we do that so once this happens there's going to be these special channels where you see these black channels here in the sarcoplasmic reticulum these black channels on the sarcoplasmic reticulum are actually going to move some of this calcium back in so some of this calcium is going to get pumped right back into the sarcoplasmic reticulum but calcium is moving against this concentration gradient because you know calcium is actually going to be in lower concentration outside the cell and in high concentration inside of the sarcoplasmic reticulum so I'm pumping it against so that means I have to utilize ATP and usually whenever you utilize the ATP in this process you're also pumping a proton out usually so there's usually going to be an antiporter like system where you're pumping a proton out at the same time you're pumping calcium ions in and as utilizing ATP that's get that's replenishing the calcium levels how else can we get calcium back in there another way that we can get calcium back in here is the calcium can't actually come over to these other channels over you see these these actual red channels here these channels can actually pump some of the calcium back in also to get some of that calcium back in but again we have to have someone to help him because he's going against his concentration grading so we found someone else and he was like hey dude no worries I'll help you out I can move down my concentration gradient and his name is sodium and sodium moves down his concentration gradient out of the sarcoplasmic reticulum into the sarcoplasm and this is an example of secondary active transport so again we got calcium back into the SR through sodium calcium exchangers were through the calcium proton ATPase is cool how do we get it back out the same channels the exact same channels so now if I take over here this black channel it's the same thing I'm going to take some of the calcium and pump it out into the extracellular environment so this is the ECF the extracellular fluid this is the protons I'm going to pump it in I'm going to have to utilize ATP okay to do this process because its primary active transport then for this one same thing I'm moving sodium down his concentration gradient and I'm moving the calcium against its concentration gradient onto the ECF that's replenishing the calcium levels back out here okay so I was trying to get your calcium levels out here replenishing the calcium levels and SR replenished so now that's going to prevent the contraction so now once that happens these calcium channels shut off calcium gets sucked back into the s are pushed onto the extracellular environment potassium channels are the primary ones they're gonna be solid ready now functioning now so potassium channels are going to even open up even more and they're going to start aggressively moving out even more so as the potassium channel start even aggress will be moving out even more again you're going to start losing more and more and more positive lines with no counteracting of the calcium so what do you expect if calcium is not counteracting this anymore what's going to happen it's going to start dropping and it's going to drop and it's going to drop until it gets to resting membrane potential and then when it drops at the resting membrane potential it'll have this brief period in time where it'll actually kind of stay rested until ions from this cell let's say a nodal cell leak into this model cordials contractile cell again via the gap junctions and that that happens what happens it goes I got to threshold potential so to finish off phase two is the plateau phase so it's kind of like cut that off right there phase one is the drop down from the potassium channels phase two is the calcium and the potassium channels these three is just the potassium channels and then we get into this last phase which is called phase four and phase four is where there is just no sodium no calcium ion movement and just potassium ions kind of leaking out very very slowly to keep it at the stable resting membrane potential until the sodium ions or other cations from the gap junctions leak into the cell again and trigger to go to threshold holy crap okay that's that now with that set we see exactly how this muscle is communicating that's the intrinsic ability iron engineer so if you guys are stuck in there throughout this entire video here where we talk about electrophysiology and very great detail I want to thank you guys enough we're gonna I can't thing you guys enough but we're going to go into part two so we talked about the intrinsic ability of the heart what I want to do now is want to go into little bit more of the detail of the extrinsic innervation of the art how that can actually bring the actual baseline of the intrinsic ability of the heart above the actual like you know basically increase in the heart rate or how we can bring it below that actual basal rate which is going to be decreasing the heart rate which is called bradycardia increase in the heart rate tachycardia so we'll talk about how the sympathetic and parasympathetic nervous system affects this activity so I hope to see you guys in part two RCC ninja nerds

Channel: Ninja Nerd Lectures

Views: 470,041

Rating: 4.9663239 out of 5

Keywords: electrophysiology, intrinsic cardiac conduction system

Id: 1kX6Tp8CWFw

Length: 48min 0sec (2880 seconds)

Published: Thu Aug 03 2017