hey everybody, welcome to part two of the chapter 20 lecture, you may remember last time we finished up with how electrical flow goes through the cardiac conducting system, remember that it started up here in the SA node, which is the pacemaker travels through the atria first, to the AV node, down through the bundle, the AV bundle here, the bundle branches, a little shortcut at the moderator band, and then out the Purkinje fibers through the lateral walls of the ventricles now, all this electrical activity can be detected at the skin, and that's what an electrocardiogram is, it's important to realize this is recording the electrical activity through the heart, it's not directly recording the contraction that's happening, if you look up in the picture in the right hand corner, we see these leads that are attached to the skin at various strategic places on the body of the patient, but we're not directly innervating the heart itself with the leads, so we are seeing basically a shadow, an electric shadow of the electric activity that is being conducted from the heart through the bodily fluids to the skin, remember that the human body is really a big bag of salty water, and those salts, those electrolytes, will conduct an electrical current through those bodily fluids, so that's why we can pick up trace amounts of this electrical activity at the skin, and again, that's what an ECG is, by the way, electrocardiogram, you'll sometimes see referred to as an EKG, from the German kardio with a "k", so again, ECG or EKG, it's an electrocardiogram, and of course this is very valuable, to get a good idea of what's happening in the heart, making sure that the electrical flow is occurring properly, the three major features of an ECG that we want to know are the P wave, the QRS complex, and then the T wave, the P wave is first, so that's gonna be this little deflection here, and as you can see that represents the depolarization of the atria, and then the atria will contract shortly after that, but again, the ECG doesn't actually measure the contraction of the atria, it just measures the electrical event, the depolarization, then the biggest feature of an ECG is the QRS complex, you can see this giant spike remember that the ventricles have a lot more myocardium to depolarize, so it's gonna be a much larger electrical event that's recorded on the ECG, so the ventricles are depolarizing during the QRS complex, and while that is happening the atria are repolarizing, they're getting set back to their original electrical state, you can't really see any different thing happening during the QRS complex that you can point at and say, oh, that's the atrial repolarization really this is all happening together, the ventricular depolarization is the main electrical event, and the atrial repolarization is a more minor electrical event that just happens to happen, that just happens to happen at the same time, and then finally we have the T wave, so the T wave will be the repolarization of the ventricles, that would be the ventricles getting back to their original electrical state, all right, so don't worry about all these technical intervals and segments, if you were going to get into a cardiac specialty, it would be useful to be able to measure some of these intervals and segments, and you would compare that to a baseline or normal value, and it can help you figure out what's going along, or what's going on, in the heart, especially with respect to the cardiac conducting system, but since this class, A&P, is not really a clinically focused class, you do not need to worry about, again, the intervals and the segments that are shown here, let's just focus on these three key features to the ECG, and what is happening during each of them... okay, shifting gears a little bit here you may remember, and I will go back and show you, for the cardiac conducting system, we talked about how there are specialized cardiac muscle cells that are represented by the purple pathway here, that are not really about contracting and squeezing blood, they're more about sending action potentials very efficiently, well, these specialized cardiac muscle cells only make up about one percent of the myocardium, the other 99% of the cardiac muscle cells that are in the myocardium are specialized to contract, so they're called contractile cells, and that's what we're going to talk about next... okay so, I'm sorry, here we go, so as I just mentioned, the vast vast majority of the cardiac muscle cells in the heart wall are these typical contractile cardiac cells, where their job is just to contract, to squeeze blood, you may remember from back in the fall when we learned about how skeletal muscles contract, some of these should sound familiar, troponin, tropomyosin, myosin, and actin, action potentials are involved, calcium's involved, all of these are true for both skeletal muscle and cardiac muscle, but there are going to be some key differences, if we look at these graphs over here in the upper right hand corner, this is skeletal muscle contraction, as we learned last fall, they have very fast action potentials and very fast contractions, notice that that means there are very short refractory periods the blue represents the absolute refractory period, and then the pinkish red represents the relative refractory period notice that the refractory periods are over by the time the contraction finishes, so that means you can have a second action potential before the first contraction even finishes, which is going to allow you to stack the contractions on top of each other to form a tetanic contraction, so let me show you just really quickly here, from back in the fall, so this is from chapter 10, and I wanted to show you this slide, just to kind of remind you, again, of things like troponin, tropomyosin, myosin, actin, calcium, action potentials, you know sarcoplasmic reticulum, sarcomeres, all of these things are found in cardiac muscle too and then if I skip ahead a few slides again, hopefully this rings a little bit of a bell, that with skeletal muscle, you can hit it with a stimulus, start to get a contraction, hit it with another stimulus before that contraction is done, and they start adding up, this is wave summation, and then you can sustain the contraction, either in incomplete tetanus shown here on the left, or complete tetanus shown here on the right, and what tetanus means is, again, you're sustaining the contraction, you're holding the contraction, for example, with a skeletal muscle, you're trying to maintain posture or you're trying to lift something and it's going to take more than a few milliseconds to accomplish that, so that's why tetanus is actually an important function of skeletal muscle fibers, but if I go back to chapter 20 hopefully it makes sense that you would not want tetanic contractions in cardiac muscle, imagine if your heart would contract, and squeeze, and just hold the squeeze, and just sustain that contraction in a squeezed contracted state, ask yourself, is any blood being pumped while the heart is just stuck in its contraction for who knows how many seconds, so that would be bad, so that's why there are these key differences, if we look down here at the bottom graphs, look how much longer the action potential is for a cardiac muscle cell compared to (what) it was for a skeletal muscle, it's about 30 times longer, and then a much more slower, sustained contraction as well here, but notice that the absolute refractory period is over, and you haven't even finished the first contraction yet, that means there's no way to really stack these contractions together to form tetanus, so again, that's going to end up being a good thing for the heart, so to summarize, much longer action potential in cardiac muscle than skeletal muscle, longer refractory periods, look how long the absolute refractory period is in blue, much much longer compared to what we saw up here in skeletal muscle, again, longer lasting contraction, which means that, again, the contraction is finishing, its already relaxing, by the time you can potentially have a second action potential, so tetanus is not possible, again, as I mentioned before, calcium is gonna play a role, in skeletal muscle, though, all the calcium that was used for the contraction came from storage, from intracellular sources, the sarcoplasmic reticulum, but for cardiac muscle, most of the calcium comes from storage, but some of it is going to come from outside the cell, as we will see in the next slide or two... here's a closer look at the action potential of a cardiac muscle cell, and you can see, you can divide it into three phases, we have the rapid depolarization phase, this is basically the same thing that we've learned before, it's when you open sodium channels, sodium rushes in since sodium is rushing in, that's positives coming in, you're depolarizing you're getting more positive, very very fast, now here's where the difference is instead of immediately repolarizing, like we saw with other types of action potentials, we enter this plateau phase, and that's because right now, you open two different types of channels, you open calcium channels and potassium channels they're kind of fighting against each other, because we have calcium that's trying to come in from the outside, you have potassium it's trying to leave from the inside, they're both positive ions, so they kind of neutralize each other a little bit, so that's why you don't really see much change in the potential positives are coming in, that's calcium, positives are leaving that's potassium, and we're plateauing, and this buys us time, it really gets this absolute refractory period really long, finally the calcium channels close the potassium channels stay open, so as the potassium leaves you're gonna finally repolarize back to your resting state, so it's really the calcium entry during the plateau that buys you all this extra time to make sure that the refractory period is long enough to prevent tetany from happening so if we were just to try to wrap this all up here with cardiac muscle cell contraction, the vast majority of the calcium needed for contraction comes from storage, it's released intracellularly from the sarcoplasmic reticulum, but about 20 percent of the calcium needed for contraction is coming from outside the cell during the plateau of the action potential, from that point it's pretty similar to what we learned last fall with skeletal muscle, the calcium binds to troponin, the troponin interacts with tropomyosin to expose binding sites for actin and myosin to contract together, and the cardiac muscle cell contracts, so just a couple more things about the refractory periods, remember that when you see the term absolute refractory period, that means you can't have another action potential no matter what during that time, and again, it's much longer in a cardiac muscle cell than it was in a skeletal muscle cell, so it's a little bit longer than the plateau phase that we saw on the previous slide, and because the refractory period goes all the way until after the relaxation phase of the contraction has begun, that prevents a tetanic contraction, which, again, is very bad, you do not want your heart to just contract and just stay contracted because if that happens no blood is moving at all... all right, so there's our bottom line, slow, long plateau phase, much longer absolute refractory period, and you prevent tetanic contractions from happening in the heart... all right, we're going to move on to the next topic here, which is the cardiac cycle, this is a simplified view of the cardiac cycle here, basically the definition of the cardiac cycle is everything that's going to happen during one heartbeat, so that means you're going to alternate between periods of when the chambers are contracting, and when the chambers are relaxing, now this being A&P, we just can't call these phases contraction and relaxation, we have to give them fancy A&P terms, so those terms are systole and diastole so systole just means contraction, so we're going to start the cardiac cycle up here with atrial systole, so the atria are going to contract whenever a chamber contracts, whenever it enters systole, it compresses, it shrinks and that puts pressure on the blood that's within there, and then the blood is going to want to squeeze out and go to the next location, the fancy term for contraction, I'm sorry, we just did that one the fancy term for relaxation is diastole, so after the atria have finished their contraction, their systole, they spend the entire rest of the cardiac cycle relaxing, in diastole immediately after the atria contract, the ventricles then do their contraction, so ventricular systole, and from this point right here, the entire rest of the cardiac cycle, all chambers in the heart are relaxing until we get back to atrial systole again, the key thing with diastole is that's filling time, that's when the pressure is relaxed, it's expanding and getting larger, which means the pressure is dropping, which means blood is filling that void and entering the chamber, so pressure is really a big deal here, I put it in all caps, blood always flows from areas of higher pressure to areas of lower pressure, that's called a pressure gradient, that's kind of just a standard rule of physics, is that gases and fluids move from areas where they're under higher pressure to areas where they are (under) lower pressure, so generating pressure is the key to understanding how blood flows through the heart, and really through the whole body, and then, as I mentioned in the last lecture, the heart valves do not open and close due to muscular contractions by the papillary muscles, the heart valves open and close based on pressure differences on either side of the valve, that will hopefully make more sense here on the next slide, as we talk about that, so again, valves are going to open and close based on the pressure differences around them, and this whole thing has to be coordinated, you do not want atrial systole and ventricular systole to happen simultaneously, or overlap in any way, the atria need to finish their contraction, they need to finish delivering all the blood to the ventricles, before the ventricles can start contracting and start ejecting blood out to the body, so let's expand upon this figure and take kind of a more detailed look at all this, so here's, again, a more detailed look at the cardiac cycle, again, we'll start up here at the beginning of atrial systole there's a lot going on here, we definitely do not need to memorize any like, milliseconds, that each of these phases are taking, I just want to kind of highlight what's happening and why it's happening, so if we start here at the beginning of atrial systole, it shows the atria contracting, and then that's going to increase the pressure in the atria and force the blood down into the ventricles, but most of the blood that enters the ventricles doesn't do so during atrial systole, we have to back up a little bit during ventricular diastole the blood that's returning to the heart through veins, that's entering the right atrium and the left atrium, it just flows, mainly due to gravity, right down into the ventricles, so most ventricular filling is actually passive, the atria aren't involved in contracting at all, for the vast majority of ventricular filling that happens, I like to think of what happens during atrial systole, is just topping off the tank, it's like saying, hey, you're almost all the way full anyway, let's just squeeze a little bit more blood into you before you start to contract, so that's the best way, I think, to think about atrial systole, so again, the atria, they have a pretty easy job, they're just topping off the tank of the ventricles, and then, again, the atria relax the entire rest of the cardiac cycle, now let's take a look at ventricular systole, so the ventricles begin contracting, as kind of shown by these green arrows, that's going to start squeezing the ventricles and raising the pressure in here, as the pressure starts to raise, or rise, it forces the blood back up against the AV valves, and forces them shut, even though the papillary muscles and chordae tendineae aren't shown here, you know that they are providing some tension to prevent these AV valves from prolapsing, or everting, back into the atria, for this brief, just few milliseconds of time, blood is not moving anywhere, the volume is not changing, because all valves are shut notice that the semilunar valves have not opened yet, so this brief, fleeting moment of time, when all the valves are shut during contraction it's called isovolumetric contraction, it doesn't last very long, because as the pressure continues to rise in the ventricles, the pressure becomes greater in the ventricles than in the pulmonary trunk or the aorta, so that means that the blood forces the pulmonary valve open here, and the aortic valve open here and blood always wants to go from higher pressure to lower pressure, so the blood rushes into the pulmonary trunk from the right ventricle, and it rushes into the aorta from the left ventricle... okay, that's ventricular systole, now we enter ventricular diastole, the ventricles begin to relax, as they begin to relax they begin to open back up again, which means the pressure is dropping well, fluids always want to flow from high pressure to low, so the fluid actually, the blood, in the pulmonary trunk and the aorta, gets sucked back towards the ventricles, that's where the semilunar valves come in, the blood gets caught in the flaps of both of these valves, it forces those flaps together and the blood cannot get sucked back into the ventricles, now, as the pressure continues to drop in the ventricles during ventricular diastole, and we start getting venous return back into the right atrium and the left atrium, the pressure starts rising in the atria, once the pressure is higher in the atria than in the ventricles, it's going to force the AV valves back open, and we're back to kind of where we started, which is passive filling of the ventricles during late ventricular diastole... oops, I skipped over this, there is a brief few milliseconds in time, called isovolumetric relaxation, where once again, all four valves are shut, so just like we saw over here, where all four valves were shut during contraction, here all four valves are shut during relaxation, but again, it does not last very long, because very quickly the pressure rises in the atria enough to force those AV valves open, and start that ventricular filling in a passive way... all right, so hopefully that makes sense, the basic mechanics of the cardiac cycle, now, you can track all these pressure changes, and what's happening, and your book has provided a really nice graph to really tie all this cardiac physiology together, now, it can seem a little overwhelming at first, there's a lot going on here, and that's why, as usual, I put this little yellow box, no need to memorize everything you see, let's just kind of take away what we want to take away from it, let's start with the easy stuff, let's start with the ECG, we've already looked at that there's our P wave, there's our QRS complex, and there's our T wave, remember that the P wave was atrial depolarization, that's the electrical event, right after that the atria should contract, that's atrial systole, same thing here, the QRS represents ventricular depolarization, so right after the electrical event should come the contraction, ventricular systole so that's the top part of this, that's relatively straightforward, let's go down here to the bottom of it which is showing volume changes, now, everything you see on the graph in the pressure area and the volume area is showing what's happening on the left side, the same things are happening on the right side, only the pressures will not be as dramatic, remember how the right side of the heart, the right ventricle, only has to pump blood to the lungs, so the pressures do not need to be as high, the left ventricle has to pump blood through the systemic circuit, which is everywhere else in the body from head-to-toe, so that's why the pressures are greater on the left side, and that's why they show the left side pressures here because they're just more exciting, they're larger, they're more interesting, but again, these volume changes that we see down here at the bottom are happening in both the left and the right ventricles at the same time, so what I wanted to really show you down here is, first, look at this passive filling, so all of this blood that's coming into the left ventricle is happening during ventricular diastole so, this is just passive filling, and then finally, when the atria contract, we're gonna top off the tank, so that's what we see over here too, here's passive filling, passive filling passive filling, and then when the atria contract, you just give that little, boop top off the tank, so hopefully this graph makes it very clear that the majority of ventricular filling is happening passively during ventricular diastole, so these terms, hopefully they make sense, what's the amount of blood that you have in a ventricle at the end of diastole, that's the end diastolic volume, or EDV, now you go ahead and squeeze the blood out of the ventricle, that's ventricular systole, so you're squeezing the blood out, but not all of it, there's gonna be some left over amount of blood still in the ventricle typically, since that's the amount, the volume, of blood that is in the ventricle at the end of systole, it's the end systolic volume ESV, so hopefully that makes sense, if you take the difference between EDV and ESV, you get stroke volume, SV, it's just simple math, the larger number, subtract the smaller number, you get the difference, that's how much blood is being ejected per heartbeat, stroke volume... all right, now, let's take a look at the pressure part of this graph, which is definitely the most complex, we definitely do not need to know all eight of these steps in order there won't be questions like that on the exam, but let's just take a look at what's happening and see if it makes sense, so the blue line represents the pressure in the left atrium, the red line represents the pressure in the left ventricle, notice how when the pressure is higher in the atrium than it is in the ventricle, that's when we're getting that passive filling from the atrium to the ventricle, now the atria finally contracts, atrial systole, so it should make sense that the pressure in the atrium, you get a little bump of pressure, because it's contracting, well, it's squeezing blood into the ventricle, so the ventricle gets a little surge of pressure that mirrors it, all right, we just topped off the tank, now, the big event the ventricles begin contracting, quickly the pressure in the ventricle exceeds the pressure in the atrium here, remember that valves open and shut based on pressure changes, so as soon as the pressure in the left ventricle is now greater than the pressure in the left atrium, that slams that AV valve shut right now all valves are shut, so we're in this very very brief moment of isovolumetric contraction, the aortic valve is still shut until the pressure in the left ventricle rises above the pressure in the aorta once it does, blood starts rushing out and through the aorta, that surge of blood creates a pressure spike in the aorta, so the pressure in the ventricle and the pressure in the aorta kind of mirror each other through this whole peak, but the ventricle starts running out of blood, right, we're kind of running out of blood here, so as the pressure is dropping in the ventricle finally the pressure in the ventricle is now lower than the pressure in the aorta and that's what causes the aortic valve to slap back shut, remember, negative pressure, pressure that's going down, is suction, it's trying to suck the blood back in, but when the aortic valve shuts, that keeps that from happening, right now we're in a brief moment of isovolumetric relaxation, where all the valves are shut again, but as soon as the pressure in the left ventricle then drops below the pressure in the left atrium, that's going to open that AV valve back open, and that means we can begin our passive filling again, so, it's not too bad if you just kind of apply some common sense to what's happening with the pressure changes driving valve closing and opening, and then the volume changes that are happening as well... so there will obviously be a few questions on the exam asking about some of these concepts, but make a list of your questions, and be sure to ask them soon so that you can get them clarified in your mind... all right, speaking of valves opening and closing, that's kind of our next topic, those are the heart sounds, and there are two main heart sounds, there's S1, or sound one, and S1 happens when the AV valves close, so when you hear that lubb sound when you're listening to somebody's heartbeat, that's sound one, that's the AV valves shutting, and then sound two, which they call dupp, is when the semilunar valves close, so that's the aortic valve and the pulmonary valve, so that lubb-dupp, lubb-dupp, lubb-dupp, signifies those valves shutting, so that's why a doctor or a nurse would want to listen to somebody's heart, because if those do not sound, oops, sorry about that, if those do not sound sharp, if they don't end with a good buh sound, or a good puh sound, that might signify that something's wrong with the valve, and you do not need to worry about exactly where you would put the stethoscope for listening to each of the valves, that's more of a clinical application, but I thought I would include it in the notes here because it is kind of interesting... notice that there are also two additional minor heart sounds, sound 3 and sound 4, they do not directly have anything to do with valve closure, and they're usually pretty imperceptible even through a stethoscope if everything is okay, so we will not focus on those, so let's just focus on S1, which is lubb, and S2, which is dupp, and again, S1, sound 1, AV valves shutting, and sound 2 is when the semilunar valves are shutting... all right, now this figure, you may like it, you may not, I'm not a big fan, it's trying to illustrate those volumes I mentioned a minute ago, the end diastolic volume, the end systolic volume, and then the stroke volume being the difference, it's trying to illustrate those by using this water pump analogy, so read through this, if you like this, use it, honestly, I think, if I just skip back, to me, I personally understand these volumes better by looking at a graph like this, but here are the full definitions, again, end diastolic volume, or EDV, is the amount of blood in a ventricle after relaxation after diastole, so this is gonna be the larger number, and then once the ventricle has contracted, and squeezed out as much of (the) blood as its going to, the amount of blood that's left over is the end systolic volume, the ESV, take the difference between those two, and that's your stroke volume, so EDV minus ESV, and you'll get a cleaner, better look at this formula on the next page, there's another way to look at how much blood is being ejected per heartbeat it's called ejection fraction, so instead of just kind of a raw volume, like stroke volume, it's saying, how efficient is the heart being right now, what percentage of the blood that's in the ventricle is actually leaving per heartbeat, so if you take the amount that leaves per heartbeat, and divide it by how much was there at the beginning, you end up getting a percentage, so usually it's around 60%, which is kind of amazing, that means that, at rest, your heart's really only at 60% capacity for stroke volume, that means if you're exercising or really working hard, there's a lot of room for this to go up, you know, your heart can start beating more powerfully, with more blood coming in and out of it and this ejection fraction will go up quite a bit as needed, so again, at rest, you still have quite a bit of reserve capacity for each individual heartbeat's volume... okay, the last major topic of this particular lecture is going to be cardiac output, so it's pretty straightforward, I think, it's how much blood your heart, cardiac, is putting out per minute, that's the definition, so there's your official definition, the amount, or volume, of blood being pumped out by a ventricle in one minute, and so here's the equation, you can see it down here as well cardiac output equals heart rate times stroke volume, so in other words, how many times is your heart beating per minute, how much blood is being ejected per beat multiply those together, that's how much blood is being ejected from your heart per minute, and just to give you some numbers, to give you some context, or reference, if your heart rate was 75 beats a minute, and your stroke volume was 80 milliliters a beat, which, both of these are pretty just average, typical amounts, for an average heart at rest, then your heart is pumping out about 6 liters of blood per minute, remember, the average person has four to six liters of blood in their whole body, so that means pretty much the entire volume of blood in your body is circulating through your heart once per minute, which is pretty incredible, I mean, the blood is really really moving, now, if you're worried about these equations and math, don't worry, I'm not going to, on the actual exam, ask you any math questions and force you to make any calculations but knowing and understanding these equations, so the stroke volume equation and the cardiac output equation, it'll be helpful for scenario-based questions that I might ask, for example, I might say, here's a variable that causes end diastolic volume to go down, how would that affect cardiac output if no other variables changed, so for example, if end-diastolic volume went down, well, if that's a smaller number, and you're still subtracting end systolic volume, so that would make stroke volume a smaller number if stroke volume is a smaller number, and heart rate didn't change, that would make cardiac output smaller, so I won't change more than one variable at a time, we'll keep things really simple, but again, if you understand these equations and what they mean, you would be able to answer those types of scenario questions where I'm only changing one variable at a time, in reality, in your body, more than one variable can change at a time, but we're not going to try to analyze that sort of complexity, so let's look at the factors that affect cardiac output, well if it affects heart rate, or if it affects stroke volume, it'll obviously affect cardiac output, so first let's talk about the things that will affect heart rate, hormones, specifically epinephrine, norepinephrine, and the thyroid hormones, all of these increase heart rate, so if you have higher levels of these hormones running through your bloodstream, that's going to make your heart beat faster, and then also autonomic innervation, so that's going to be, of course, sympathetic versus parasympathetic innervation, and we'll talk more about that on the next slide, and then we'll finish up today's lecture with talking about some of the factors that can affect end diastolic volume and end systolic volume, which, of course, will affect stroke volume, and by affecting stroke volume, that will affect cardiac output... so let's start here with autonomic innervation, take a closer look at that, you do not need to memorize the neural pathways for both the sympathetic division and the parasympathetic division to the heart, this might ring a little bit of a bell, we saw some similar diagrams last quarter when we did the nervous system, but let's just focus over here on the bullet points of this slide, again, I tried to remind you from last quarter, when we learned about dual innervation, the fact that most of our internal organs are innervated both by the sympathetic and the parasympathetic divisions, the heart obviously is too, both divisions, and then we talked last quarter about autonomic tone, autonomic tone means there's always some sort of baseline level of impulses that are going to the heart, and the cool thing about autonomic tone, if you remember, means that you get dual controls, you can change heart rate by either increasing or decreasing sympathetic output, or increasing or decreasing parasympathetic output so that's where dual innervation and autonomic tone kind of come back again from last quarter, also from last quarter, when we were learning the brain, the medulla oblongata, remember, this is the lowest part of the brain, the lowest part of the brainstem even, and we had some cardiac centers there that are really in charge, on a really base level, of regulating heart rate, so it goes like this, you have a cardioacceleratory center, which is the one shown in pink or red here, as the name implies, the job of this center is to send a message to accelerate your heart rate, to raise your heart rate, and that would be during the fight-or-flight response, right, so sympathetic input, the neurotransmitter that causes heart rate to go up is norepinephrine, we'll see how that happens on the next slide, and then the opposite is the cardioinhibitory center which is shown in blue, so if you want to slow, or inhibit, your heart rate, it would take parasympathetic activation to do that, and it's a different neurotransmitter that slows the heart down, and again, on the next slide we will take a closer look at how this happens... all right, as we talked about in the last lecture, part 1 of the chapter 20 lecture, that when you're at rest, your heart sorry, your brain, your medulla oblongata, is always sending parasympathetic input to the heart to slow it down a little bit from what it would be if the pacemaker was just working on its own, if you were to eliminate that parasympathetic input, the heart rate would probably drift up more to its natural state that the pacemaker would set, if you recall from last lecture, it varies, but it could be between sixty and a hundred, so if your pacemaker's natural pace is, like, 90 beats a minute, but at rest you're normally only 60 beats a minute, if something was wrong with the vagus nerve, it got damaged, you can no longer send parasympathetic information to your heart, the heart rate would probably go up at rest, closer to the pacemaker's natural rhythm everything, of course, is reflexively controlled down here, your conscious brain cannot change heart rate, at least directly, it's going to be due to reflexes, so your medulla oblongata down here is getting input all the time from stretch receptors in the wall of the heart, so if the wall of the heart is being stretched, that might mean that the heart needs to pick up the pace to get more blood flowing through it, and I'm gonna give you an example of that in just a second, also, the medulla oblongata is getting stimuli, it's getting input from blood pressure receptors in some of your major arteries, as well as chemoreceptors in some of your major arteries and your brain, and if carbon dioxide levels, or oxygen levels, or pH levels, or blood pressure levels, are changing, your medulla oblongata might reflexively change heart rate to try to bring you back to homeostasis with those variables, so here's one specific example of one of these autonomic reflexes, it's called the atrial reflex, named after Bainbridge, so you can also call it the Bainbridge reflex it's due to, when the right atrium is getting a lot of blood coming back through the veins, through the systemic veins, then that means that it's starting to stretch more, as I mentioned a minute ago, the stretch receptors in the wall of the right atrium send a quick reflex loop message to the medulla oblongata to say, hey, pick up the pace, I've got too much blood coming in here, we need to increase heart rate so I can get that blood squeezed down faster to the right ventricle and then back out, there's an old saying with the heart, more in equals more out, so if more blood starts coming into the heart, you have to make the adjustment to get more blood going out, otherwise everything is just gonna back up, so again, that's one specific example of a reflex, a cardiac autonomic reflex all right, so as promised, I wanted to talk a little bit about the mechanism of how the two different neurotransmitters affect the SA node, the pacemaker so the parasympathetic neurotransmitter is acetylcholine, and the way it works is it causes more potassium channels to open, so let's take a look at what this would look like on a graph, this is normal, so we saw a graph similar to this in part 1, the last lecture, where this is an automatic depolarization by the SA node, it's called the pacemaker potential, because the pacemaker cells are already very very leaky to sodium, so this is just your normal depolarization of your SA node, if you want to slow the heart rate down, look what happens, by opening additional potassium channels, remember potassium, if you open channels for it, is going to want to leak out, well that means the inside is gonna become more negative, because it's losing positive ions, so look at this, the resting potential now, when you're, when you have acetylcholine and parasympathetic stimulation, now it takes longer for that spontaneous depolarization and look, we have a slower heart rate, we've hyperpolarized, and now have a slower depolarization, we're maybe down to maybe 40 beats a minute, whereas normally we're up at 75, just the opposite happens for sympathetic input, that's going to cause the neurotransmitter norepinephrine to be released, which opens up additional sodium and calcium channels, both sodium and calcium, we have more of it outside the cell, so if you open up channels for this, more positives are going to come in, if more positive ions come in, the inside is going to become more positive, notice you've gone from a resting potential of about negative 60 to something much more positive, now the pacemaker potential is much shorter, you have a much more rapid, quick depolarization, and so it doesn't take as long to reach threshold, and now the heart rate has increased quite a bit, so hopefully that makes sense, how, by opening up certain types of channels, you can affect that resting potential, and then how fast the depolarization happens to threshold... okay, we are going to finish things out for this lecture by talking about some of the factors that affect stroke volume, so here's the equation again, as a reminder, stroke volume equals end diastolic volume minus end systolic volume, so anything that affects EDV or ESV will affect stroke volume, I don't think there's really any need for you to try to memorize a bunch of up and down arrows, I think a lot of what we're about to talk about here just makes sense, just use common sense and then by knowing this equation, you can just apply it and figure out what's gonna happen, so let's go, let's start with filling time, I hope this just makes sense, that filling time is just how much time does the ventricle have to fill, so how much, how long is it relaxing, if you have more filling time, if there's a longer period of time that the ventricle is relaxing in diastole, then, right, if you have more filling time you have more blood in the ventricle at the end of diastole so that's increased end diastolic volume, it should be noted that the faster your heart is beating, kind of by definition, there's less time in between each beat so that's why I said earlier, in reality more than one of these variables is likely to change at the same time in your body, it's just a matter of which variable changes more, and then you get some sort of net change, some sort of net overall effect in the body, but we're gonna keep our learning of this very simple, and again, I will only change one variable at a time, and hold all the other variables constant, for any scenario-based question that I would ask you... all right, so that's the first one, that's filling time, very closely related to filling time is venous return, in fact they really go hand-in-hand, because the more time you have to fill, the more you're allowing blood to return from the veins, so venous return just means how much blood is coming back to the heart from the veins, hopefully, once again, it makes sense that the more blood that's actually coming back, the more blood you're going to have in the ventricle at the end of diastole, so both of these will increase EDV, which means that if all other variables are held constant, that's going to increase stroke volume and remember, if you're increasing stroke volume, if all other variables are held constant, that's going to increase cardiac output too... all right, preload preload just basically means how much are you stretching the ventricle wall at the end of diastole, well if you have more blood coming in, and if you have more time for blood to come in, the wall of the ventricle is going to be pretty stretched, so both of these are going to affect preload, and again, this is all proportional, this is my little proportional symbol, that's what this means, proportional, so preload is proportional to end diastolic volume, the more blood you have in the ventricle, the more the wall is stretched, so you have a higher preload okay, let's now look at some factors that affect end systolic volume, let's start with afterload, now, I apologize, it's kind of a long, drawn-out explanation up here in the notes, but hopefully once I explain it, it makes sense afterload is basically the amount of pressure that the ventricle has to generate to overcome any resistance that's out there, so for example, what if like, most of your major blood vessels were constricted, it's kind of hard to force blood through a narrower passageway, right, if your blood vessels were vasodilated, there's not as much resistance to flow, but if they're all vasoconstricted, there's more resistance to flow, so if you have a lot of vasoconstriction happening, or, for example, what if you had some sort of vascular disease, where you have a lot of cholesterol plaques in your blood vessels, really narrowing them, that will increase the afterload on the heart so now the heart has to work harder to force blood out through narrower vessels so when you narrow the vessels, that's going to increase afterload, when afterload is higher, that means your heart is working harder to pump out the blood there's likely to be more blood left over in the ventricle at the end of each heartbeat, so end systolic volume has gone up, so hopefully that makes sense, the harder it is to pump the blood out that means you have increased afterload, the more blood that's left over after each beat, it's just, you can't get it all out, because it's harder, so if something causes end systolic volume to go up, can you see how that would make stroke volume go down, right, because if this number becomes higher, you're subtracting a larger number from EDV, that's gonna make stroke volume lower, if everything else was held constant, and if stroke volume goes down and everything else is held constant, then cardiac output goes down... all right, I've got one more variable here, it's contractility, pretty simple, it's just how strong of a contraction is your ventricle squeezing with, and notice that the things that affect contractility are pretty much the same things that affect heart rate, so if you have a fight-or-flight response, if you have sympathetic stimulation, not only does that make your heart beat faster, it makes it beat more powerfully, each beat is stronger, hopefully it makes sense that if each individual beat is stronger, so if contractility is greater, there'll be more blood that gets squeezed out per beat, so there's less blood left over, so increased contractility is going to lead to a lowering of ESV, if you're lowering ESV, you're subtracting a smaller number, that's gonna make your stroke volume bigger, (it's the) opposite with parasympathetic, so not only does parasympathetic stimulation cause your heart rate to slow down, it causes your heart to beat with less force, and then pretty much the same hormones that increase heart rate are the same hormones that increase contractility as well... all right, so a lot to go through there, but hopefully a lot of it is common sense, once you think about it... I'm just gonna finish up here with this kind of summary slide this is kind of taking all of the different factors that could potentially affect cardiac output, and just shows them in a much simpler way, so we have the factors that affect heart rate, mainly hormones and autonomic innervation, and I gave you an example of a specific reflex that does that, and then here are all the major factors that affect stroke volume, which were explained on the previous slide... okay, so again, these equations, the equation for stroke volume and the equation for cardiac output, it's good to at least understand what they're representing, but I will not ask you on the actual lecture exam to do any real mathematical calculations with them, because this is not a math class, and I don't think that's necessary... all right that is a wrap on chapter 20 part 2, the next lecture will be part 1 of chapter 21, make sure, as always, as questions are popping up, you're writing them down, and you are emailing them to me, or you are getting on to a Zoom session to ask them live... have a great day, and I'll see you next time