in the heart function on Tuesday we looked at sort of a brief anatomy of the heart we looked at where all the conductile components of the heart are located essay node AV node conductile fibers we took a look at what all that has to do with EKG readings and electrodes because when you look at the heart you know it's good to study it sort of individually so you get solid with the details but you need to you know be able to look at it sort of as a holistic organ that can function uh in times of um you know high oxygen man demands for cells and low oxygen demands for cells so we're going to see how it does that on this particular page as well as details about really two main types of cells make up the heart we have what are called work cardiomyioes and these are they're called the work cells because these are the ones that when they contract they generate force and that force is used to pressurize blood so that we can get it to move in the correct direction because we know that blood moves with pressure high pressure to low pressure when we look at cells in the heart 99% of cells in the heart are contractile cells or work cardiammyio these are going to be striated cells they have a lot of similarities to skeletal muscle cells which I'll talk about they have some unique features as well so we'll sort of compare and contrast pacemaker cells these are the cells that generate action potentials only 1% of cells in the heart are considered pacemaker cells what is the pacemaker of the heart essay node so when we talk about pacemaker cells the essay node should be the cluster of cells that's producing the heart rate should the essay node become damaged and it can't do its job or perhaps the interodal fibers that connect the AV and the SA node maybe those are damaged and the AV node doesn't get information in any case the AV node can take over as the pacemaker of the heart if the essay node can no longer do it the AV node is sort of like second in command sort of like your backup um option there the problem with the AV node is that it cannot generate a very fast heart rate about 40 maybe 50 beats per minute would be the max and so that would allow a person to survive but they're not going to be able to move around or exercise a lot so that would definitely be a time where maybe the person would be eligible for a pacemaker that's usually where pacemakers are sort of installed to to help overcome the fact that the essay node can no longer do its job so just a few things to be aware of unless I say otherwise when I talk about pacemaker cells I'll be talking about the essay nodes so just be just to be aware unless I specify otherwise that's what I'm talking about so sort of wrapping all that up into our pre-class um not review but just some things that you'll hear me talk about on this particular set of notes main function of work cardiammyio this around didn't quite get this set up just right main function of work cardiammyio is to they contract they shorten and they generate force and that force again is used to pressurize blood so that we can get it to move in the right direction pacemaker cells let's talk about pacemaker cells um pacemaker cells in the essay note again that's what I'm mostly going to focus on today um they are cardiomyioytes but they don't have sarcimeir so they're going to have a similar shape and size they're going to be short fat and branched but they look clear if you looked at them histologically it's because they don't have any sarcimeirs because they don't need them that's not their job they don't contract they just depolarize so the main function of pacemaker cells is to spontaneously depolarize and what that really means as far as a more functional sort of view spontaneously deolarized means they generate action potentials before anywhere else in the heart can even get the idea that maybe they should generate action potentials the SA node not only generates these action potentials through spontaneous depolarization but because they are able to depolarize and generate action potentials a little bit faster than other areas of the heart they should suppress other cells from even getting the idea that maybe they should generate their own action potential and this is sort of an like a not often discussed or sort of focused on detail but I think it's important so the AV node can generate an action potential bundle of his bundle branches they can all generate action potentials even work cardiammyioytes can generate their own action potential so if you don't have sort of an overriding force or leader that comes in and says we will all beat at the same time then those other areas of the heart could start generating their own heartbeat that's called u an ectopic heartbeat you have different areas of the heart generating action potentials at different times that is horrible for blood flow because you don't have an accumulation of cells doing the same thing at the same time so blood flow is disrupted you can't generate enough force maybe you don't get ejection into the aorta for example and so being able to suppress any idea that these other cells are going to even try to deolarize on their own is really important really important so um it's it's not just spontaneous deolarization and creation of action potential it sets the pace for the entire heart and what that truly means is it prevents other cells from generating their own action potential all right so on this um set of notes here what we're going to do we're going to look at two sort of distinct sets of cells we're going to look at work cardioes we're going to see uh location and um structure and then on the right side of the piece of paper we're going to look at pacemaker cells also their location and structure so we're going to take a look at the 99% of cells in the heart and then we'll talk about the 1% of the cells that keeps them all together so that's where we're headed i'm going to set this back up i always thought that the essay nodes job in addition to you know generating action potentials when we think about controlling all the cells of the heart it sort of be like uh hurting cats trying to prevent all these other cells from trying to generate their own action potential really really important so let me get this set up here we're gonna kind of make the leap between anatomy that we saw in lab a few weeks ago and some more cellular details we're going to find that the heart thinking about the heart wall here which is what I'm going to sketch over there you can sort of ignore that drawing for a moment it doesn't really need much right now but the heart wall whether that's atria or ventricles doesn't matter but we'll see three distinct layers in the heart wall anywhere in the heart wall three distinct uh tissue layers is what we're talking about here the heart has some complexity in its walls some things that you probably would expect to find and a handful of things that you might not be expecting to find um here are the names of our three layers we're going to see endocardium myocardium and epicardium these are the three layers and if you'll look at their prefixes you can kind of get an idea of where these layers reside endocardium obviously lays on the inner sort of layer of the heart wall endo my means muscle and so myioardium is the middle layer it's the muscular layer that's where we actually find the contractile cells don't epicardium epi means surface when you dissected your heart specimen in lab weeks ago and you looked at the surface of the heart assuming you didn't have your paricardial sack covering it but let's say you got rid of the paricardial sack if it existed and you're looking at the surface of the heart this sort of gleaming sort of watery surface that was epicardium so you've actually seen epicardium uh you just might not have known that's what it was called so just the surface of the heart when we think about what are these layers made of we see some pretty distinct differences come about so [Music] endocardium is made of simple squamus epithelial cells or simple squamus epithelium myioardium made of cardiammyio so those would be the work cardio the ones that contract generate force and then our epicardium is also made of an epithelial tissue but it's a little different the epicardium is made of a special epithelial tissue called meothelium meothelium it lines the a lot of the organs in the body it lines some of the cavities it is technically a specialized form of simple squamus but me you ever heard of a cancer called meotheloma that's that's the tissue that becomes cancerous so about 85% of all cancers are epithelial in origin epithelial tissue by nature goes through mitosis a lot it divides a lot it pairs a lot of cells and whenever you have a set of tissues that is naturally meant to go through mitosis a lot go through a lot of cell replication you can see how things could get off a little bit so epithelial tissue both good and bad as far as its ability to regenerate simple squamus epithelium it's been a while since we talked about that we saw that in our first lab of maybe second lab of the semester what would that look like hisytologically remember small and flat yeah flat nucleus one layer thick so this simple squamus epithelium is an interesting tissue it looks like really thin tiles so this is it simple one layer thick squamus flat epithelial tells us it forms some sort of barrier or lining and so we can get a sense for the shape of cells based on the nuclei and then it would be supported by a basement membrane but that's it so this simple squamus epithelial tissue or epithelium uh is continuous throughout all chambers of the heart so the atria the ventricles uh tbvicular carne papillary muscle all the features we found in the heart they're all lined with this kind of um slick tilelike layer cells and this is continuous with blood vessels so we have ideally a very continuous lining to all parts of the cardiovascular system and the benefit of that is that it reduces turbulence what is turbulence you ever experienced it in an airplane was it fun no not unless you're you know really looking for adventure um but turbulence and blood flow is really bad because it's sort of the antithesis to flow so if we had uh a blood vessel and some of its epithelial cells were just going to draw a little like diagram in here let's say one of these epithelial tissues or cells was sort of sticking up and impeding the lumen so we should still have this nice flat epithelial tissue but if we can't keep these epithelial cells stuck down then it can provide turbulence so instead of having nice blood flow we may get some sort of eddy or some sort of disruption to flow and any resistance to flow is bad right the opposite of flow is resistance and so what that does is not only create turbulence in the blood flow it can create little microbubbles microbubbles can be bad because they can actually plug small capillaries but any resistance uh can increase workload on the heart because the opposite of flow is resistance and so we hopefully we don't have that i just wanted to mention that because it's just really easy to kind of take this for granted and say "Okay it's lined with the stuff and that's that's me but what like who cares?" And so once you realize the physiological significance of not having this it's kind of substantial so bring that up myocardium again work cardioes uh this layer the cardiomyioytes here these are going to be the area or the part of the heart that generates uh force or pressure so usually we say muscle cells create force but in the case of the heart we're really trying to pressurize blood and then we're back to the epicardium the mesothelium again a specialized simple squamus epithelial tissue it would look similar to this but it would be on the outside part of the heart so I'm going to just sort of introduce if we took a a portion of the heart let's say we cut out a little part of the ventricle atria would have the same setup but if we were looking at a ventricle we would see endocardium mocardium epicardium and we would see that the myioardium is by far the thickest we would see some similarities between endo and epicardium and then I wanted to add in just the details remind you of the paricardial sack and fluid that should be surrounding all that so just to keep it sort of straight go ahead and kind of go through this and then ask you some questions about why why is it like this what what's the point of all this so here is our ep or excuse me endocardium this is our [Music] endocardium made of our simple squamus epithelial tissue in the middle myocardium where do you think the mo myocardial wall or portion would be thickest what chamber over four left ventricle that's right so the mocardium may change substantially in thickness and that just reflects workload of that chamber we should not see change in thickness of endocardium or epicardium these should be relatively uniform throughout the heart they should all be simple squamas and then we're back out to the sort of the outside part of the heart see if we can recall the sort of features of of our paricardial sack aka paricardium what is the outer layer of our paricardial sack called very outer layer give you a hint kind of looks it's got some structure fibrous this is our fibrous fibrous paricardium that's the very outer layer what is right inside or lining the fibrous paricardium yeah the parietal layer of the cirrus paricardium or just simply the parietal layer or parietal paricardium going to abbreviate there then we have uh moving deeper we are into the paricardial cavity the paricardial cavity contains the paricardial fluid that's this right here and we talked about the volume of fluid somewhere between 20 and 60 ms hard to know for sure the ideal because of how we get that data usually the person has been uh you know through some sort of trauma so it's probably going to disrupt the actual fluid volume and then what is the inner layer of this called the cirrus of sirus paricardium of that cirrus paricardium but the visceral layer visceral layer of cirrus paricardium so visceral because it sits on the outside of the heart so visceral usually means something about an organ so this is our visceral paricardium so the heart wall has a lot of you know structure and features and some of that is outside of the epicardium some of it's in the middle so thick walls full of cells that require a lot of oxygen where do you think the myioardioes the work myioardio in here get their oxygen from these are obligate aerobic cells cannot go without oxygen where are they going to get that from think about when you cut through that ventricle how thick was it inch maybe places possibly half inch so I'm going to repeat the question how do those cells in the middle of that get oxygen so if this is the you know if this was the left ventricle I'm just going to use that as an example we have oxygenated blood cells sitting right inside that chamber don't we if you're cardioite here Can you access that oxygen you cannot two reasons one that's a really thick diffusional distance you're not going to diffuse oxygen from the cell to the mioardioes at a rate that's that's going to sustain them two endocardium is a type of epithelial tissue it forms a barrier its job is to prevent diffusion of things from a chamber into the cells also the chamber sometimes doesn't have blood right sometimes it's empty sometimes it's filling sometimes it's pressurized sometimes it's injecting and so it cannot permit or allow oxygen here to get into here so how are we going to answer how are we going to get oxygen to those work cardioes in the middle of this myioardium how does any cell or tissue get oxygen blood vessels there are so many blood vessels in that myioardium so many and their job is to oxygenate those work cardiammyio what happens if you have a blockage in one of those main vessels what does that cause what does that cause you got a blockage in a main vessel that's a heart attack that's what a heart attack at the cellular level physiological level is you've got a blockage in the large blood vessel and that large blood vessel either fed or actually weaving through these workio if you have a blockage there how did those cells get their oxygen well they don't and so they die and that's called a moardial inffection that technically is a heart attack and so when you think about blood pressure keeping your blood vessels free and clear of you know atherosclerosis there's a whole lot of reasons we want to connect that back to prevention of a heart attack it's because the heart itself takes a lot of oxygen and if your blood vessels that feed those cells are blocked you're not giving those cells oxygen and they don't put up with very long not having oxygen and so that is an irreversible cell death cardomiotes when they die they they don't come back and so that part of the heart is no longer functional and so how much of those cells die where that blockage was how far up that blockage was can determine how big was the heart attack was it a small heart attack and a small cluster of cells die or was it a big heart attack a fatal one but lots of cells went without oxygen for too long and too many of them died for this heart to be able to be functional again so there's a lot of connection between generating force and having enough oxygen for yourself to do the job is that why you can still be conscious and kind of that you're having a heart attack as well like your heart is hurting like it's like you're slowly dying yeah so a lot of people um actually can have a heart attack and not know it they don't know they've had a previous heart attack until they go to the doctor and they do some sort of acid test and the doctor finds evidence of a past heart attack if it's a small cluster of cells you don't know and so that can become a larger problem larger problems become a big cluster of cells but a lot of times the heart pain of angina is what you're talking about so that's called is due to cells not getting enough oxygen sort of like when your muscles burn you're exercising too much they don't get enough oxygen that's what angina is if you're feeling that you're in sort of dangerous territory as opposed to having small cluster of cells you really good but you wouldn't have the same same symptoms lots of things to think about as far as connecting heart structure heart pressure and blood flow to you know things that are common problems that people have things that we have to put up with as far as you know being human humans are known for cardiovascular defects and you know they think you know you hear a lot about oh modern lifestyle is what's causing it we don't exercise enough we don't eat well but they've actually found evidence of atherosclerosis in people that lived 10,000 years ago these were hunter gathers they walked everywhere they ate the freshest food because they just killed it themselves they too had atherosclerosis we think atherosclerosis is a problem of homo sapiens we know that other primates also have aosclerosis so you see certain diseases run in certain clades of of vertebrates it's an interesting thing doesn't mean we can solve it any easier but it's interesting to think about so let's talk about within the mioardium what we've just talked about um I'm going to talk about two things one kind of already talked about blood and lymph vessels but in that moardium that's where we'd find our conductile fibers if we were talking ventricles for example that's where we'd find the perkingi fibers that's how the perkingi fibers tell those cardiammyioytes hey know your time to deolarize they run through those cardiammyioytes branching many places if we were talking right atrium what would those conductor conductile fibers be called interotal fibers if we were talking left atrium what would those conduct fibers be called bachman's bundle or Bachman's branch there aren't there's not a there's not a redundancy sort of system there if Bachman's doesn't work then there's not a lot of ways we're going to get that information to the left atrium so myioardium more than just work cardiammyioytes we have things that tell the cardiammyioytes now's the time to deolarize and contract and then we have you know routes of nutrient and oxygen delivery we also find lymph vessels in the myioardium before I leave the idea of blood vessels have to flow through the heart wall to feed the cells when do you think blood peruses those cells during diastily or sisily say it again when we talk about feeding cardiammyioytes work cardiammyioytes i'm going to go back up here maybe a sort of an image would help i'm going to use sort of a contrasting color here's our blood vessels all sorts of blood vessels so many blood vessels weaving through this myioardium trying to feed all these work cardioes that are obligate aerobic cells when does flow happen through those vessels during diastily or cy diasty the answer is diastilly because when the heart wall contracts it produces a lot of pressure but it closes off those vessels blood vessels are soft tissue they're easily squeezed these capillaries are just one cell layer thick anyway you squeeze a capillary flow through that capillary stops let's bring this back to talked about earlier why is a slow heart rate to a point good what are you allowing to happen in the myioardium that might be benefited from a slower heart rate to a point i'm not saying you should have like a heartbeat of 20 beats per minute what's that to speak with a neural human to So the ventricles are filling with blood but in regards to blood flow to the mioardium why is a slow heart rate beneficial yeah that's right the longer you spin in diastin the heart wall the longer you're not pushing on those capillaries and accluding them so the slower heart rate is healthy because you in turn get more blood flow to these capillaries in turn supplying these work cardiammyio with more oxygen this is one more connection exercise is medicine people that consistently habitually exercise usually have a lower heart rate at rest and that allows over time you know days weeks if you look at how much more oxygen their heart cells got that's quite a bit so a lower heart rate to a point is very good a lower heart rate below too low is not good because other cells of the body are not getting what they need so profusion of the myocardioes really an interesting thing to think about and really now you kind of know on a very very basic level kind of the the pathophysiology of a heart attack which is something you know it's like one of the top three killers in this country right up there at diabetes for example okay let's talk about what we just talked about so I did that I was a little bit ahead of myself so question one make sure you can summarize what we just talked about and answer question one how does flow through these blood vessels that we looked at up here change between diia and cy so make sure you can answer that comfortably so when we think about these work cardiammyioytes they have a big job they have to contract and that's going to generate force and as I mentioned earlier force here is all about pressurizing the blood within a chamber this is a big task this is more than what we're asking in some ways skeletal muscle to do because all of these cardiamytes have to be polarized at just the right time based on what something else perhaps far away said they have to act as a sensitium you ever heard that word before sensitium a sensitium it refers to a large group of cells acting as one so if you think about the billions of cells in the heart the heart scales proportionally with your body it's about the size of your fist and if you you're asking all these cells to work together as one to make a coordinated heartbeat that's a big ask we don't ask all of our skeletal muscles in the body to work at the same time that would be fatal but you just don't see that and yet we just sort of have the heart do that day in day out and we usually don't spend much time thinking about it so when we ask the heart to ask is a sensitium again a group of cells working together to accomplish a common goal like the heart it's not just that they have to work together and stay coordinated but we need them to change their activity in a coordinated way to answer what the body needs the heart works for the body's cells meaning if the body needs more oxygen the heart will be asked to work harder so the heart works for the body cells not the other way around it's not that the heart beats at a certain rate and the body kind of has to just put up with that that's not how it works so in addition to generating force as a unit they have to be able to change their force that they generate based on what the body needs and that is called contractility so contractility you can think about it as how forceful uh the the pressure is that's been generated we can change that peak force at a given time we do that by changing the myioite length cardiac muscle cells these work cardioittes have a weird habit in that if the more you stretch them the more force they generate frank Starling law of the heart we can see how that works if we fill a ventricle with blood the more blood we put in that ventricle the more stretching those cells have to undergo and they will respond by contracting harder so it's an interesting system if you have high venus return back to the heart you've got a lot of blood flow coming back to the heart it's going to stretch the ventricle and those cells respond by contracting harder that's called contractility and this whole idea is explained by something called the Frank Starling two people law of the heart the more you stretch these cells the harder they contract this is an interesting thing to think about it makes sense the only reason you'd be stretching them is because you had more blood return to the ventricle and the other reason you have more blood return to the ventricle because your body needs more oxygen so it's sort of a selfserving cycle that allows the heart to pump at a a force that is equivalent to the amount of blood returning back to the heart and that all has to do with the fact that these cells change their length and respond by contracting harder so we're going to see the structure of work cardiammyioytes get an idea for how they are able to accomplish many of the things we talked about and I'm going to give you a few uh we're going to look at three cardiammyio i'm going to add a lot of detail as you can see over here can move this up so we're looking at three work cardioes we're going to add some details that you can see on the side we'll talk about sort of the strange shape that they have the number of nuclei and their location it's very different in skeletal muscle cells talk about what's internally and what we find inside these cells my fibbrals sarcomir lots of organels and how these cells communicate with each other which happens at an area called interpolated discs some of these heart cells have two nuclei some have one it is not completely out of the question to find heart cells that have three nuclei but they don't have hundreds like skeletal muscle cells had skeletal muscle cells had hundreds if not thousands of nuclei we're not going to see that in these cells these cells become multi-ucleated if they're going to be multi-ucleated they become multi-ucleated in a very different way compared to skeletal muscle how did skeletal muscle cells become multi-ucleated was it during fetal development perhaps yeah so this is a reminder skeletal muscle cells become multi-ucleated because they fuse you have myoblasts that fuse form a myotube the myot tube then forms into a multi-ucleated skeletal muscle cell cardiac muscle cells very different they actually start the process of mitosis so they undergo nuclear division which means you get from one nucleus two but they don't get to complete cytoinesis so they undergo nuclear division two nuclei they don't complete cytoinesis you can see how it almost looks like this was able to split apart but it doesn't so that's how you can get sometimes two or even three nucleus nuclei per cell not all of them do that not all of them go through nuclear division so let's talk about some things that we're going to see here i'll be adding details inside and out so I'm gonna move this up so you can see the details so we'll be starting um just sort of an overview of these cells they work as I mentioned before as a sensitium which means these should all get the message to deolarize and contract at the same time even though they are three different cells these cells the shape of cell they're very short they're usually pretty um pretty thick they have a pretty thick diameter and they are often branched and that branching actually allows them to communicate with many many neighbors so I just have this one communicating with two other cells in reality it's not unusual for a single work cardioite to communicate with 11 other cells so it can have a lot of neighbors but um just drawing it sort of as a sequence like this is a little bit easier so the nuclei of work cardioytes is usually centrally located as opposed to skeletal muscle cells remember how we drew them and the nuclei were seemingly sort of poking up from the bottom you could almost see the nuclei it looks like they made the saroma look bumpy that's not the case with these these are just centrally located more like an average cell i'm going to talk about some stuff on the outside before we do the details on the inside so the surface of this the cell membrane is still called a sarco lima so that is similar to skeletal muscle it is a phospholipid billayer so we still have a pretty um good membrane surrounding these we're going to see that between neighboring cells is an area called an intercolated disc and this is one of those points that a lot of people just um kind of blank out on on the exam so this region here that I'm dotting that region is called an intercolated disc it contains structures but the region is called an intercolated disc things we would find in any intercolated disc a region between two neighboring cells a really important one are gap junctions gap junctions are something we looked at a while ago back in the first module of this semester so if we need a refresher on what gap junctions do check that out gap junctions are true proteins they're structures and gap junctions act like uh tubes or conduits that allow items to flow from the inside of one cell through this to the next cell gap junctions permit what is called an electrical synapse we haven't really seen electrical synapses we've seen chemical synapses where one cell released neurotransmitters those neurotransmitters diffused across the clft and were received by receptors on the other side that's a slow process comparatively electrical synapses um just allow a lot of sodium for example to flow from one cell to the next and this allows the deolarization or action potential in this cell to easily very quickly depolarize this cell which would then depolarize this cell this is key in having these cells act like a sin sysium the flow of ions is pretty much continuous and uninterrupted we don't have to wait for neurotransmitter release and then diffusion and then receipt that's a very slow process compared to this so action potentials seemingly slip and roll very quickly through the heart allowing ions to be shared in fact you could trace an ion if you had the ability you could see it the same physical sodium ion here flow through all these different cells so those are gap junctions located in an area called intercolated disc so intercolated discs um allows sodium to move without diffusion it doesn't have to go through our extracellular fluid environment what I'm kind of coloring in here these cells like any cell are surrounded by bathed in whatever descriptor you want to use there ECF extracellular fluid and so having a conduit or tube that allows things to be shared between cells without having to first diffuse through your extracellular fluid medium is really really helpful so they can share ions they can share small metabolites it's not just for sodium things of a certain size or certain diameter can easily fit through those scapul so again is a key to allowing these cells to act like a sin sysium i'm going to talk about things we're going to find inside of these cells now are there any questions on sort of outside details questions all right inside of these uh work cardioes is amazingly strikingly similar to skeletal muscle cells we're going to see that the internal volume is largely taken up with myopibbrals i'm just going to draw a few of those here i'm sort of short of space but we'll see lots and lots of myofibbrals what do you think we find inside myophibbrals myofilaments good and they are arranged in circum so this is why cardiac muscle cells are considered to be striated just like skeletal muscle cells myophibbrals containing sarcimeirs now some of their myophibbrals may run at an angle to fill the cell so they don't have to be quite so rigidly arranged but they still fill the majority of the cell's volume and also the myofbral arrangement allows the cell when it contracts to sort of contort and twist which is what allows that ventricle or atria to contort and twist you know when the heart beats it sort of rings and part of part of that is due to all these cells having myofibbrals running at different angles really filling up the majority of that internal volume so myophibbrals with sarcimeir other things we'll see associated with are myopibbrals label that down here in case that's not super obvious when you're studying later myophibbral with sarcimeirs and we know sarccomirs contain myofilaments actin and meioyosin but surrounding the outside of this we would still have sarcoplasm reticulum and surrounding that we'd still have reticular mitochondria so I'm not going to attempt to draw it this is way too small for me to do that but again it's the same setup of skeletal muscle directly surrounding my fibros coposite reticulum and they release calcium directly surrounding cycoplasiculum reticular mitochondria and they produce ATP also we're going to find just like skeletal muscle cells our sarmma is going to invest or um sort of take a dive in i'm going to use this cell as my um model here and we'll see that the saroma forms T-tubules just like we saw in skeletal muscle cells so this is what I'm drawing here t- tubules transverse tubules where the saroma allows that extracellular fluid to come all the way through and that's going to allow for an interaction of myofibbrals and that tubial wall so tubules here same as skeletal muscle we still have type calcium channels here we have myopiberal here we see the RS so intracellular details here very very similar to skeletal muscle all right the only thing left on my list to talk about would be myoglobin what is the purpose of myoglobin what does it hold on to or store oxygen and remember work cardiammyioytes are obligate aobic cells that means they can't produce enough ATP at all without oxygen they don't handle uh you know glycolysis very well they don't have the enzymes to do that to the degree they need so obligate a means they need a constant amount of blood flow in order to produce the ATP needed and we saw up here how do they get that blood flow well they get it from all those blood vessels that flow through the myioardium so obligate aerobic cells must have not just enough blood flow but usually they have enough myoglobin that holds on to that oxygen sort of stores that oxygen so this is our example or sort of sample I should say of stuff about work cardioes the ones that are doing a lot of the work in the heart questions before we continue yeah other questions we look at the cells that are coordinating all of this hurting cats the cells that you have right in front of you here that you drew that you see here these could if they don't get any information they'll start to generate their own action potential but they don't do it in a way that's coordinated they'll say different things like different rates i think this should happen do I think this should happen and now all of a sudden you've got ventricles with different rates of contraction within the same ventricle that's pretty dangerous questions as well so an electrical synapse is only where we see sodium flow from one cell to another so TuS would not do that they would be full of extracellular fluid and the action potential will come down but they would not be responsible question so I've not heard of that a lot of it has to do with how the the heart forms during fetal development it's the first organ to form and it actually forms like a figure eight so the sort of the cartilage skeleton of the fetal heart already sets these cells up to be arranged at oblique angles so I I don't know that you would have a viable heart like the fetus would not continue to develop if there was something wrong with that sort of figure eight arrangement so that's a good question yeah oh the myoglobin oh that's a good question where is myoglobin so myoglobin is actually pretty small and it would just be you know I'm just going to sort of dot it in anywhere there's room so myoglobin is very small myoglobin um just fits in between different parts different organels for example uh myoglobin you've you've heard of hemoglobin that's sort of its corlary in the blood we know uh you know we know what hemoglobin is myoglobin is a funky thing i'm just going to um ask you a question when we think about myoglobin uh versus hemoglobin just to connect this to things that you already know about myoglobin just has it's a big globular protein but it just has one iron core whereas hemoglobin is a tetrammer it has four iron cores so if you looked at myoglobin it's just going to have one area iron it's the red here whereas hemoglobin has four so myoglobin can only bind or hold a single oxygen molecule whereas hemoglobin can bind and hold up to four oxygen the funny thing about myoglobin is once it binds that oxygen it holds on to it really tightly it binds it um more easily than hemoglobin does and it holds on to it more tightly uh it does not give oxygen up to the blood myoglobin's kind of greedy like that what I really mean by binding and holding is we could look at something called an oxygen saturation [Music] curve and you know if we had really low oxygen in the blood hemoglobin is not going to be very good at holding on to it it's going to give it up myoglobin though can bind to oxygen at a really low rate and it binds it quite well and holds on to it so myoglobin really reaches saturation quickly and it holds on to it if you compare this to hemoglobin so myoglobin is kind of like hyperbolic in shape if you looked at hemoglobin it's more sigmoidal it takes it a while to finally bind and it binds a little bit slower and then finally it will catch up to myoglobin but when you look at the oxygen saturation curve of these different globular proteins maybe that better graphs maybe that helps you understand myoglobin binds oxygen at a lower saturation and the blood holds on so it doesn't give up whereas hemoglobin starts to give it up nice thing about hemoglobin though is the tissues your oxygen level starts to decrease will lose oxygen to the cell that's what it's designed for so it's not like this was just you know not made as well it just has a different purpose and sometimes when you sort of display when you look at this hyperbolic curve versus this more sigmoidal curve you can kind of understand the benefits of having two different proteins that bind oxygen so thank you for that i apparently had a lot to say about that um we are going to move into though details of essay nodal cells get this set back up and be on our way we're going to talk about the tiny cluster of cells that is the essay node is not very big in fact it's so small that when the SA node depolarizes you won't find an EKG wave that is specific to SA node you'll find the Pwave so we know the SA node to deolarize but the Pwave does not represent SA nodal depolarization directly so SA node considered to be the primary pacemaker of the heart primary pacemaker is the SA node syoatrial node so the term pacemaker what does that mean you had to explain it to someone that wasn't sure what does pacemaker mean yeah sets the heart rate yeah so it regulates it sets it that's good so pacemaker means it's going to We could go even a different route it's going to determine heart rate which I'm going to abbreviate HR and it should do it better than other cells so they never get the idea that hey maybe I could take over today no somebody's got to be in charge and we hope it's the essay node otherwise we have trouble so what does pacemaker mean it is the cluster of cells that determines heart rate and we can change this we can change how this works and we're going to see how this works based on this example this is a scenario SL question so to see how the heart works as far as setting its rate changing its rate responding to different homeostatic needs of the body remember heart rate itself is not a regulated variable we want it to increase and decrease we're about to talk about how it does that so in the absence of any autonomic nervous system influence meaning sympathetic and parasympathetic if we had no autonomic influence no neurons telling the SA node what to do we would find that the SA node would prefer to fire at a rate that yields 100 to 110 beats per minute at rest would that be a high resting heart rate yeah what's average for an adult about 72 you know it's going to be higher if you're older a little bit lower if you're younger but on average 72 is considered average resting heart rate now if the essay node is left to to sort of function on its own it's going to do so at 100 to 110 beats per minute that's pretty high and that's wasteful and it's hard on the heart so again this is if we eliminated autonomic tone sympathetic and parasympathetic so what does that tell us about autonomic nervous system or ANS tone at rest remember essay node would like to be or would prefer to be 100 i'm just going to say 100 because it's easier but resting heart rate 72 70 72 so at rest which way does our autonomic tone slider go does it go more towards sympathetic or more towards parasympathetic parasympathetic this is a way to look at this idea called rest and digest which we've seen before you know parasympathetic tone means you're relaxed you call it rest and digest this is one way that happens if you're not stressed out nothing's chasing you just sort of watching TV for example you're going to find an average resting heart rate and that's because the sympathetic tone is much higher if something scares you bust through your door and demands all of your iced coffee i mean them spite words right so your sympathetic tone is going to go up and consequently your heart rate goes up so we can see this relationship by looking at a pretty basic graph and usually when we talk about parasympathetic tone you'll see it called veagal tone what do you think that's referring to vagus nerves good so veagal tone is literally the same thing as parasympathetic tone when we're talking about heart rate so I'm switching words on you and I know some of this like well that's annoying i don't disagree but the vagus nerve cranial nerve 10 is the cranial nerve that intervates a good part of the heart remember cranial nerve 10 is strange i mean it's name vagus which means vagrant which means wanderer it wanders around in the thoracic and even abdominal cavities it hits a lot of different innervates a lot of different organs so when we talk about veagal tone we're talking about the vagus nerve which houses parasympathetic neurons so that's why you see the word bagel up here so 100 beats per minute that's what I was talking about this essay node generates 100 beats per minute if you don't have any autonomic tone information autonomic intervation has been eliminated and so what we can see we talk about sliding scale 60 beats per minute that's pretty high veagal tone pretty low heart rate 100 beats per minute that's pretty high and then you can kind of see how this fits in the middle so as sympathetic tone increases heart rate increases as veagal tone increases heart rate decreases it's also a good way to remind ourselves that never on this sliding scale no matter how you draw like this or just like a sliding scale it's never zero or 100 you can't have 100% parasympathetic tone and zero sympathetic tone you would not live so we can see one might be high one might be low but they're never going to be zero there will always be at least a little bit of that intervation happening vagel tone strange word but that's what it means questions where's the essay found within the three layers of the heart oh that's a good question it's going to be a little bit in the myioardium so epicardium you can think of as protective surface one layer thick endocardium sort of an inner barrier slick tilelike lining one cell layer thick so the SA node usually lives a little bit closer to the endocardium than epicardium if that helps uh that's a good question Sydney when we also look at perkingi fibers a lot of times you'll find them right between the endocardial moardial boundary as far as the big ones anyway so good question other questions before we continue i'm just going to talk a little bit about the structure of the essay node it's tiny it's so important for controlling so many other parts of our physiology so we've mentioned this before where is the essay node located now remember it's a tiny cluster of cells you could dissect a lot of different hearts and you're not going to see it but we know from you know electrical measurements where it exists we've also seen that the essay node when we did our drawing on Tuesday is located in the superior and somewhat lateral wall of the right atrium so RA for right atrium it is near the junction of the superior vennea opening and where the oracle the right oracle sort of so your superior vennea comes down into that right atrium and you've got your oracle sort of that ear sort of on the it's like a flap hanging off the front and the side but right at that junction where the oracle and super superior vennea come together that's usually where we find that essay node in most people if we were to describe the structure of the node it is a very tiny of a crescentshaped cluster of cells so sort of like a a moon shape sort of a crescent moon shape these cells the essay node remember they they're modified they look uh clear which is another reason why they're hard to find they don't have a lot of internal structure that even stains well with H& so they're hard to find they are technically though modified meioytes just no sarcimeir so they start life as a meioy just like a cardiammyioite but the sarccomirs do not develop so they're clear if we were to look at their structure just gonna sort of highlight this over here this is um kind of a just a basic sketch of what an essay node looks like there's really three populations or types of cells that we need to think about when we think about the essay node so part of the shape of this node is given to us by this it's got a layer of connective tissue and it kind of forms what this node's going to look like and so this layer of connective tissue helps orient your essay nodal cells again they look like cardiammyosittes they're just kind of empty looking but their sort of basil surface or basement area is going to be supported by this connective tissue and that causes their uh sort of branches to face outwards and that's good because when these deolarize it points the action potential that leaves it points it in the right direction so out here is going to be the lateral aspect of our right atrium up there the superior aspects of our right atrium we already have this design such that when these cells spontaneously the polarized action potential can only go in one angle it sort of points it out in the right direction the first cells that these orange or SAL cells are going to deliver their action potential to these are all connected with gap junctions just like we saw over here but circulated disc with gap junctions um the first population of cells that we're going to get are called transitional cells so I'm going to sort of introduce this if I can get this to fit in so here's our SA nodal cells and our SAL cells are able to transmit that action potential that they generate to a very small subset of cells called transitional cells and these only exist to sort of link our essay nodal cells with our first conductile fibers some essay nodal cells and you can kind of see how this is is going to work just based on their their position to each other so sodal cells depolarize hand it off to a very small subset of cells called transitional cells and then we're going to hand off to what might be cardiammyioytes they can serve as conductile fibers believe it or not but we'll just keep it pretty simple and call these are the conductile fibers and so we'd be off and running getting that wave of deolarization flowing in the right direction towards that left atrium or sort of angled down towards the AV node which is the next target i think we'll stop there this is a good We only have like seven minutes left um so this is where we'll end for your exam material that you're responsible for for next Tuesday it's a good amount of stuff to go through you probably already knew that so the review tomorrow again I'll do sort of a a scheduled review where I go over old exam questions we'll I'll then take questions from you if you have them it's kind of what you want to make of it is totally fine otherwise I will see some of you tomorrow i'll see the rest of you on Tuesday feel free to contact me if you have any questions no because it's during lab i don't record a twohour lap that would be Yeah right i'm so glad we also have