Transcript for:
Physiology of the Heart

hopefully you learn from skeletal muscle you learn from the neurophysiology and now all we're going to do is we're going to take those procedures and modify it slightly for the heart okay now you all learned what an action potential is right an action potential is when you have opening a voltage-gated sodium channel sodium comes in and you get a depolarization then uh they close because they're on a timer three milliseconds later right uh the voltage against sodium channels closed voltage-gated potassium channels open and then you have the repolarization that depolarization repolarization then is an all-or-none event and the next part does this the next part does this the previous part doesn't because it's in a refractory period so you get what's called a wave of depolarization that goes along right that's all review when we talk about the heart they don't have traditional action potentials that is called a spiked action potential because it looks like it goes up to a point then it comes back it doesn't have a spiked action potential inside of heart so the muscle tells inside the heart i mean remember skeletal muscle has these action potentials and it's these action potentials that go down the t tubules to open the voltage-gated uh calcium channels on the sarcoplasmic reticulum to release the calcium right i'll review that should be in your head like no tomorrow right okay well i'm just going to tell you some differences now between the cardiacs so take that process but instead of a spiced action potential we have what's called a plateau potential and i did do this in lab too the plateau potential the difference is in addition to uh potash voltage-gated potassium channels opening you have voltage-gated what not voltage-gated what opening calcium voltage-gated calcium opening but it's not quite as quick as the sodium and all of that so you get some calcium coming in but the calcium coming in is positive and the potassium going out is is positive so we have positive leaving but positives coming in so we have something that's trying to repolarize the potassium right because positives are leaving but then we have something depolarizing that's the calcium coming in so the result is instead of you depolarizing and then repolarizing back in a normal action potential or spiked we depolarize and because you're during repolarization you're also depolarizing you have something like that so here we have sodium going in and then here we have potassium going out right here we have sodium going in and then here we have potassium going out but also calcium going in so positives going in positives going out that slows it down so it doesn't go bad it re-polarized right away so we have a modified action potential this is called a what plateau potential why because it looks like a little plateau or a little table or a shelf there now the result of this is that now you have two sources of calcium inside of a muscle cell instead of a cardiac muscle cell a skeletal muscle only has one source of calcium that one source is the sarcoplasmic reticulum but the cardiac muscle cell has two sources of calcium they still have a sarcoplasmic reticulum you still have um these uh plateau potential plateau potentials triggering the opening of voltage-gated calcium same process as you learned in skeletal muscle it's just that you also get extra cellular calcium calcium is coming from the outside so you have two sources of calcium and the reason why you have such a much more long period of depolarization and why we have these plateau potentials is now the refractory period will be longer right remember the fracture period you have to kind of get back to normal before you start again the refractory period is longer now why do you want a refractory period longer because you don't want to go to tetanus remember what happens you can actually stimulate faster than the contraction and relaxation so in your regular muscle i can keep it contracted meaning though even though my signals go one every three milliseconds it takes longer to contract and longer to relax than that so i can stay contracted that's tetanus and then what happens when you go to tetanus for a long time you fatigue well we don't want that happening to your heart you want your heart not to stay locked in position whether it's locked open or locked closed won't do you much good you have to a pump has to change volume in order to make the blood move so we want a long refractory period in order to prevent the tetanus so the refractory period instead of being like three milliseconds it's 250 milliseconds that will then prevent tetanus so we have these plateau potential and plus the extra calcium coming in will lead to a stronger contraction right more unlocking of the troponin tropomyosin so basically if you know muscle for skeletal muscle all you do is modify it a little bit and now you know heart which is what i was trying to get at right so the only thing we have now is an extracellular source of calcium and of course that delays the repolarization phase so that extends the refractory period and it then prevents the heart from going into tetanus and if you don't go into tetanus of course you won't fatigue you have time to make your atp you have time to continue to do that so that's why it's very aerobic remember we do lactic acid fermentation right when you are going so fast that you can't make your atp using cellular respiration well it's the depolarization and the depolarization when you're trying to repolarize that's what delays it and that is caused by calcium but really what it is is the fact that you haven't restored back your membrane potential back to normal remember it's a signal so you turn on the signal you have to turn it off before you turn it on again so you're taking a long time with your signal on so you can't start the next signal until you finish that unlike a regular action potential which is like three milliseconds for your thing so you can actually stimulate faster than it takes to contract and relax so you can get a sustained contraction you don't want that for your heart you don't want to go like this if i go like this not going to pump have to change volume like if i take a pipette and i go like this am i going to be squeezing any water out or anything no you have to squeeze let it fill and squeeze to get it out right you have to change the volume so the heart doesn't work normally it works different than skeletal muscle but it's still based upon the same principle same troponin tropomyosin blockade same atp myosin head attaching same you know same thing except we have a little bit of modification so once you learn the skeletal muscle just extend it a little bit with these new little concepts and now you understand how heart muscle works okay so they still have a creatine kinase remember i told you the first step is your immediate reserve all that stuff still applies and in fact we can identify heart attacks because their enzymes even though they do the same thing they are slightly different in form there are different forms so when you have a heart attack those cardiac enzymes because the heart attack is when your heart cells die right your heart cells die they release the enzymes into your blood and then they detect the cardiac enzymes to detect if you had a heart attack the more cardiac enzymes they have the more cells were broken so that's why they do blood tests to see if you had a heart attack and by the blood test results they can see how bad a heart attack you had meaning how many cells got killed you know fancy name of course would be a myocardial infarction right so what they're looking for is cardiac enzymes cardiac enzymes like creatine phosphokinase and the troponin tropomyosin that's that's in the heart the cardiac version of those those versus the skeletal muscle version and you shouldn't see that in your bloodstream to large amounts unless of course you have death of the cells so do you understand that no it's not beating a lot faster i mean i can move my muscles faster it's beating slower but it is continuous and you don't want it to fatigue my muscles move a lot faster than my heart i mean my heart you know the signals for my muscles can happen as quickly as one every three milliseconds this is one every 250 milliseconds so basically i can have four signals to my heart per second i can have like 333 you know i mean whatever you know 300 odd signals to my skeletal muscle in a second and i told you the reason for that you don't want your your you don't want to fatigue your heart and you want it to change volume that that is what it is so that's all this first part is saying you know then the absolute refractory period is 250 milliseconds versus two to three for skeletal muscle right um okay another difference is that what is needed for skeletal muscle to start the action potential right the action ultimately it's an action potential that causes the release of calcium from the sarcoplasmic reticulum right the action potential causes the opening of the voltage-gated calcium and the calcium goes from the lumen of the sarcoplasmic reticulum to the sarcoplasm you all know that right well what is causing that in the heart oh first of all what's causing it in the muscles well at this point you should know and what it would be is a signal from the motor neuron that signal is ach right ach causes the postsynaptic potential which then depolarizes the threshold which triggers the action potential i told you guys by this point you should know all this stuff okay so it's ach you need a signal from a motor neuron and that motor neuron could be activated because of a reflex or it could be activated because of your cortex i want to move my hand or boom it's moved right whatever the reason is ultimately it's a signal from a motor neuron that is not required of the heart i don't need a motor neuron to tell the heart to contract or not it doesn't need acetylcholine now does it have acetylcholine there yes because nerves can modulate the heart meaning slow it down parasympathetic or speed it up sympathetic but it doesn't need it i can take out the heart put it in a jar nutri nutrition and it'll be it on its own if i take out your muscle put it in a jar of nutrition it will not unless i shock it or unless i put a motor neuron that i stimulate right won't happen it won't just start contracting i need to stimulate it somehow well not true of the heart okay so another difference is that the cardiac muscle doesn't need external stimulation the heart itself has special cells called pacemaker cells that generate the rhythm so the heart has pacemaker cells that will generate the rhythm another difference is that the junction between skeletal muscle and the motor neuron is chemical synapses but in heart muscle it is electrical synapses now what did i tell you the advantage of a chemical synapse is you have more regulation more versatility but electrical synapses you have more speed and coordination so you can synchronize activity and that's what you want you want the cells to contract at the same time remember i told you if you're stuck in the mud on a bus if i push and then you push and then everybody pushes not going to go anywhere but if we all push at the same time you'll get somewhere right same thing so you want the activity of the heart to be coordinated or synchronized that's why it has the gap junction okay that's why it has electrical synapses synchronization of activity okay but you do lose something in versatility that's why most of our synapses happen to be chemical but in the heart synchronization is more important because of the force you want to pump properly remember i told you it's also like rowing you know more important like is the timing you know that everyone is synchronized in order to get a good efficient flow all right same thing so we have uh these gap junctions and we have cells that can generate the rhythm on their own now these cells generate electrical signals called pacemaker potential now so far we know what electrical signals are and we talked about several we talked about action potentials normal action potentials are spiked we also talked about now a plateau potential which is a different electrical signal see this one involves a calcium current we also talked about postsynaptic potentials before remember epsps ipsps and we also talked about receptor potentials they're they're uh graded potentials that are caused by a stimulus for instance like this uh the electrical signals that you get when you cut when you make the hairs move on a hair cell or the electrical signals that you get when a photon of light hits a rod right that will then affect the current and affect neurotransmitter release so we talked about different kinds of electrical signals now we're going to talk about another one a pacemaker potential the pacemaker potential is present in what cells the pacemaker cells of the heart and they are used to generate the rhythm where's all my shock freaking weekend like a year ago i hid some chalk up there and it worked it's still there well i didn't remember until just now i'm like oh yeah didn't i hide some chalk up there all right and it works don't tell anyone i think i still have some chocolate here too i put them up there because every time i have to i have like i put a whole bunch and then it just disappears i really think someone is calcium deficient taking them and eating them there's other ways to get calcium people you don't have to eat the chalk all right drink more milk all right so we have the pacemaker i guess it would help if i turn on the light okay pacemaker potentials in a pacemaker potential we have our resting membrane potential right all of these cells have a resting membrane potential but in a pacemaker potential or in the pacemaker cells the resting membrane potential is not stable so instead of staying at at the resting membrane potential it gradually drifts up to what threshold remember what threshold is what's threshold no that's threshold voltage for a muscle now that's different than threshold threshold is the point in which voltage-gated channels are going to open now normally we talked about thresholds for action potentials that's the point where the voltage-gated sodium channels are going to open but in these pacemaker cells threshold is not voltage-gated sodium but it's voltage-gated calcium so at this point calcium voltage-gated calcium are going to open and you're going to depolarize it's going to close on a timer then potassium is going to leave and you're going to repolarize okay now it kind of looks like an action potential right it kind of looks like an action potential but instead of staying at the resting you drift up to threshold again and then you go instead of staying at resting you drift up and you go and so we have this rhythmical electrical activity that's passed along by the what well these are the pacemaker cells they're passed along via gap junctions so this depolarization are going to go through gap junctions causing depolarization to threshold which then causes the plateau these are the cells of the heart that make the contraction these are the cells that cause the activity that makes the contraction so it's not a neuron acetylcholine that's causing you to go up like here we have like acetylcholine and skeletal muscle or we have a postsynaptic potential of some other cell so it's not that in this case it's the electrical activity of these guys that are causing depolarization to get this right right and so the and they are done by gap junction okay gap junction now why in most cells do we have a resting membrane potential and why do these cells just happen to excite themselves they are self-excitable they right they they don't need a signal to do this they're just exciting themselves they see themselves in the mirror and are impressed huh these are pacemakers no that junction is how these two things are connected no no the electrical signal is generated by these pacemaker cells and these signals are called pacemaker potentials the pacemaker potential is what allows the depolarization of the contractile cardiac cells to start the plateau potential and this plateau potential is what causes the actual movement so the excitation that starts the plateau potential is caused by the pacemaker cells and their pacemaker potentials and those pacemaker potentials are transmitted to the cardiac contractile cells via gap junction okay yeah um that happens after this this signal is what triggers the myosin heads and all of that happening the pacemaker cells are used to trigger the plateau potential the plateau potential is what triggers the release of calcium and all from two sources this triggers the release of calcium from the sarcoplasmic reticulum and it triggers the release of calcium or the influx of calcium from outside so you have two sources of calcium now remember it was this action potential in in the skeletal muscle which then went down the t tubules to cause the release of calcium calcium binds to the troponin and tropomyosin remember this was the signal that caused that well in cardiac muscle this is the signal not this this plateau potential is the signal and what causes this plateau potential well what causes the action potential in skeletal muscle is acetylcholine released from a motor neuron what causes this excitation is a pacemaker potential from a pacemaker cell that is transmitted not via a chemical junction like here but via gap junction so you see them in the heart are they around the heart they are in the heart they are part of the heart and they they actually they're all throughout the heart but the ones that are fastest happen to be in an area that we call the sinoatrial node and then there's also another part called the atrioventricular node but these cells these pacemaker cells go throughout that's why if you have damage to the sinoatrial node or the av node your heart will go out of whack because other cells will start to take over the rhythm and make the pace okay so the normal pacemaker cells now we have tons of pacemaker cells but we have some that are the fastest and because they're all connected by gap junctions the fastest ones will trigger the rest okay unless of course there's conduction problems scar tissue or something then you could have an ectopic focus meaning you have competing centers and you have arrhythmias and all kinds of pathology but under normal condition if these pacemakers don't now i want to go over the mechanism of why these guys are unstable why is it that everything else needs to excite to get the threshold and these guys excite themselves what sympathetic comparison pathetic is modulation of this this is not this doesn't need any input i'm saying it's doing it on its own now how did we get a resting membrane potential we learned this we have three mechanisms the sodium potassium atpase pump closed sodium channels at rest no that's what it is but the three mechanisms are potassium leakage channel closed sodium channels at rest and sodium potassium atpase pump remember i told you that's how we started this and then you're going to need to know it for here now those three mechanisms there are slight differences between normal cells and these pacemaker cells well they still have the sodium potassium atpase pump because you still need to maintain the potassium levels but these guys don't have the same leakage channels the leakage channels for potassium are even slower so you know normally potassium slowly leaks out well these guys are even slower now why are they even slower well because you don't want the potassium to over compensate for the sodium now remember i told you sodium channels are normally closed at rest in these guys they have sodium leakage channels so sodium slightly leaks in and the reason why you have to make the potassium slower is because the sodium leaks in and then potassium leaks out you'll get no effect so you make the leak of potassium even slower and a leak of sodium comes in so as sodium is coming in what's happening to the membrane potential is getting more depolarized till it gets the threshold then you open the voltage get calcium and a whole bunch of calcium comes in and you get super depolarized then it closes on a timer and then potassium repolarizes it but then because sodium is leaking in slowly and potassium's leaking out even more slowly so it doesn't come that you gradually go back up to threshold and the process repeats so the mechanisms that normally maintain the negative resting membrane potential are different in these cells they are different in these cells these cells have a don't have closed sodium channels they have a sodium leakage channel and the potassium leakage channel is even slower than normal because you don't want the potassium leak to compensate for the sodium leak so you have an even slower potassium leak right leaking in positive leaking out they'll cancel so you have a slower one out a little bit of a leak coming in and so you slowly go to threshold which means that what happens you trigger the volt opening of the voltage-gated calcium and you get this plateau potential okay so do you notice that all we did is we took things that we already knew and we added a few different details and now we got this and that's that's exactly what i was trying to get to before so now we went through actually half of these notes already that's that's all the difference is so once you know the principles you still apply those principles and just add a few different details and remember there's a reason for this there's a reason we have the pacemaker potentials with gap junctions it synchronizes activity you don't need external stimulation right uh there's a reason we have this calcium current it gives you more calcium and it also gives you a longer refractory period so you don't go into tetanus so they have different physiology because they have slightly different functions right you don't want to be able to contract now my hand i don't want to have to let go of something all the time maybe i want to hold something or maybe i want to sustain it so you should be able to go to tetanus but you don't want that for your heart right you don't want that so slightly different functions you're going to need slightly different mechanisms and like i said can you alter this yes what can happen is these cells can get inhibited or these cells can get excited so that they're faster so even though they don't require a stimulation i could what if i put a neurotransmitter that actually makes it even more depolarized that means that even with their unstable they'll be going faster and that's what happens when you are under sympathetic stimulation you want it to go faster and likewise what happens if i put neurotransmitters to cause eps ipsps then even though it's unstable it'll take longer to get to the top so then it slows it down that's what happens under parasympathetic so even these guys you can modify but even if you did nothing they would still generate a b so you could modify them with ipsps and eps fees but and that's what the sympathetic and parasympathetic does but you don't need to they can have their own rhythm all right does that make sense i told you we're gonna go over stuff and i expect you to know the past stuff so that we can just go on yeah so after explaining those things why is it that you can take the heart of out into the heart because the heart includes these old but these pacemaker cells if i take out the heart it generates its own rhythm because they have these pacemaker cells i don't need a nerve coming into it that's what no i i said if i take it out and i put it i i said if you take it out and put it in a jar of nutrition like with oxygen perfusion whatever it'll last for as long as you can nourish it i mean you know as long as you can nourish it i mean even when we do transplants i mean a heart you can take it out and it'll survive or else you couldn't do a transplant of course what we do is we don't keep it beating what we do is uh you slow it down and you know put it on ice or whatever it stops and then you prevent it from getting damaged and then you do it again yeah yeah calcium channel blockers will affect the rhythm by affecting this okay they'll affect uh calcium channels and so you can use them to regulate your heart rate and to regulate uh these irregularities so you can see where calcium channel blockers may affect right all right so heart can beat with me completely without nervous input no no no system special algorithmic cells the heart condition impulses that's what i just do there gap junctions a couple of pacemaker potentials i already go there i already told you the mechanism for pacemaker potential but we really went over all this blah blah blah blah blah here is the sequence of excitation i told you the sinoatrial node has the fastest pacemaker cells so they generally drive the rest know this pathway yeah at least three points or so oh now you say which one before you didn't care which one now do you think i'll be asking at least a multiple choice on how pacemaker potentials work and how a plateau potential of course okay just come on unless you want me to make it a written question no no but this is different this is uh this is this pathway this pathway from the sa to the a b av to the atrioventricular bundle or the bundle also called the bundle of hiss to the right and left bundle of his branches the purkinje fibers that's just from anatomy that's easy excitation that's why i said it'll only be like three points there's no explanation for that that'll be like one of the written come on there's no explanation so a simple list like that because i'll probably say lift the excitation starting with the sino-atrial and ending with the purkinje fibers so all you have to do is throw an av atrial ventricular bundle and right and left bundle of his branches only three points because there's no explanation if i put an explanation yes it will be fixed on the right just the stuff on the there's only two words here this is where they're usually fight for two words how's that long it goes from here to here now if i add the explanations for all these which are here then we will make it more points like right there three more points three more points three more points six points almost a percent in the class right eight points is the percent in the class so six points trust me you'd rather have as many points that you know about rather than not you're like i don't want to do this okay then that means more multiple choice but you have no clue do you not understand the strike you guys are things so you guys are you don't you don't pick good strategy i haven't decided but i told you some explanation already i said if they node it has the fastest pacemaker cells those are the ones going to drive the other rhythm av node actually delays the impulses to give time for the atria to finish contracting because you want the atria to contract together and you want the ventricles to contract but you don't want the atria and the ventricle to contract at the same time so you want to synchronize the atria and synchronize the ventricle the ap node actually delays the impulse so that to give the atria time to finish contracting before the ventricles are stimulated the bundle of his just transmits those impulses to burkinji fibers which go to the uh contractile uh muscles of the heart that's the explanation oh that was it it wasn't it wasn't hard i haven't decided yet but if i do that's the explanation okay i just went over it i said i haven't decided not but the explanation is right there and i just told you verbally so yes yes yes so anyway uh special considerations the for wave excitation as they know it causes contraction of right or left contraction begins at the apex of the heart why do you begin at the bottom well that's because all the major blood vessels are on the top so you start squeezing at the bottom so that the blood will be ejected superior bundle of his is the only link between atrial and ventricular contractions so if you screw that up uh like with scar tissue or damage then you will have trouble regulating your heart rate in fact that's called av block that was a quiz question i think somewhere no yeah all right well there you go so i told you we did some of this in lab all right uh arrhythmia is when it's uncoordinated now why would be uncoordinated if you have different pacemaker cells or you don't have proper coordination between them fibrillation what's fibrillation rapid and irregular contraction reduces efficiency why if i go like this to my my uh pipette am i going to be able to squeeze anything properly no i have to change volume efficiently if i go like this it's not going to much is not going to be coming in and it will be hard for me to transfer anything right remember a pump you have to change volume let it go suck it up change volume again release it right if i go like this hardly anything's going to be coming in and out and i can't fill up my test tube right well that's your heart you don't want it to go like this you're not going to have it efficient you're not going to be able to pump okay and in fact that you may have heard of a defibrillator right have you ever heard of a defibrillator a defibrillator what it does is it depolarizes the entire heart and hopefully then by depolarizing everything these guys will start to take over and then you'll regulate it back so the problem is of course large currents can damage the heart but then again if your heart is about to stop anyway you know so don't do it for fun don't just go hey oh maybe okay so you shouldn't do it for fun but but what the theory is if you're having all these irregular centers you force them all to go depolarized at the same time and then the fastest one should take over and then drive the rest of course if you have some pathology where they're uncoordinated it may then go back or whatever but that's how you think or if the heart is stopped you try and stimulate these cells to try and get them to go again okay all right uh ectopic focus is when other rhythmic cells other than they say no take over extra systoles when outside influence leads to premature heart contractions so certain drugs may then cause these contractions to occur at different times hard block av node or bundle is not transmitting the sinus rhythm to the ventricle sinus rhythm is when the sinoatrial node is driving the contraction that's the normal condition so you go to the hospital and they go oh you have sinus rhythm that's a good thing that's normal if they say you have nodal rhythm that means that the av node is controlling it not the sinoatrial node and it's supposed to be the sinoatrium external innervation regulating heart function heart can be without although parasympathetic and sympathetic do control to do regulate it right it can't modulate it parasympathetic goes from the cardio inhibitory center also located in the medulla as well as the um what we talked about the vasomotor center before remember so that was also in the medulla oblongata then you have the vagus nerve cranial nerve number 10 going to the heart this releases acetylcholine and acetylcholine will cause ips in these pacemaker cells then we have the sympathetic it increases the rate of contraction from the cardio acceleratory center also in the manual lateral horn of the spinal cords of preganglionics of t1 t5 to the post ganglionics of the cervical and thoracic ganglia to the heart what this does it causes epsb's speeds up the pace pick up the pace right of course we already know what ekgs are because we did it in class so you already know the p q r ast right we did it in lab so we don't have to go over all that again you should know pr interview interval in fact you have to calculate that remember when i told you to count all those little boxes each one is point zero four seconds so you should already know all this stuff from last okay uh qt time of ventricular contractions systole is what we call it when the heart is contracting diastole when it's relaxing cardiac cycle all the events of systole and diastole during one heart flow cycle events of the cardiac cycle oh okay no this is actually basically anatomy but i'm going to ask you this too because it's so important to the process although this one will probably be a 12 pointer now you're paying attention 12 points out of 200 okay eventually but it'll be all of this now normally i'm gonna explain it to you right now normally i i like you to use it in your own words but this is so long if you don't do it right it'll really piss me off so for this one and this one only maybe just write it you know but if you can't explain in your own words and you'll do it right then of course use your own words okay but i want you to include all these details like when the valves are open when they're closed what happens to the pressure blah blah so basically we have different phases mid to late ventricular diastole that's when you're going to fill up the ventricles that's when the ventricles are filling with blood of course the av valves have to be open because that's the only way to get blood from the atria to the ventricles because you're filling up the ventricles here the pressure is low in the chambers but high in the aorta and pulmonary trunk because you just pump blood uh through there so it's low in the chambers of the heart meaning that blood will want to go to the chambers um the aortic pulmonary semilunar valves are closed in order to prevent backflow because the pressure is high in the odor and pulmonary trunk you have to close the semilunar valve or else the blood will go back there and we do want blood to fill it up but not from where you just where you don't want to fill it up from where you pumped it from you want to fill it fill it up from the previous part you want to fill it up from the vena cava right and from the lungs the pulmonary into the left atrium you don't want to fill it up from where you pumped out blood okay so blood will flow from the vena cavas and the pulmonary vein into the atria blood flows through the av valves into the ventricles passively that's about 70 that's why if you have atrial fibrillation it's not as immediately life-threatening it does screw up the efficiency of your heart and it could cause you to have an enlarged heart cardiomyopathy and problems you know long term it can cause you to to have severe heart problems but acutely if you have atrial fibrillation it'll just affect your efficiency but it really won't stop your heart but if you have ventricular fibrillation that's when your heart stops so atrial fibrillation because 70 of the movement is passive anyway you don't really need to pump as much uh however when you do pump the remaining 30 percent of the blood is going to go so definitely if you screw up that pumping action you'll screw up a significant portion and it will lead to long-term problems but acutely some most of the blood will go through passively anyway atrial diastole which is the relaxation of the uh the atria will occur through the cycle so you had atrial fiscal and atrial diastole while the ventricles are still in diastole then we have what's called ventricular systole that's when you're going to eject the blood from the heart after filling it up so this first stage is when you're filling it up this stage is when you're going to get rid of the blood from the ventricles remember the atria are the chambers that receive blood the ventricles are the chamber that send blood so the ventricles will begin to contract and the av valve will close why do you close the av valve to prevent the blood from going back to where it came from where it came from it just came from the atria i don't want it to go back there i wanted to go forward board means into the aorta and uh what pulmonary trunk right you want it to go forward so you close the av valve to prevent it from going back but remember the semilunar valves are still closed because the semilunar valves are still closed you want to make sure what happens to the pressure if i have close semilunar valves closed av valves now the volume of blood is not changing like blood is not entering and blood is not leaving so the volume of blood is the same so we call this the isovolumetric contraction phase but what happens is i i'm not changing the volume of the blood but i'm changing the volume of the chamber i'm contracting so what's happening to the pressure remember boyle's law volume is inversely proportional to pressure so as soon as i contract the pressure is going to go up the pressure is going to go up so much in the blood that is going to burst open the semilunar valves and then the blood is going to go into the aorta and pulmonary trunk that's called the ventricular ejection phase so the semillon valves will open and they'll go into the aortic pulmonary trunk then we start the process of filling again the ventricles are going to relax ventricular pressure becomes low the semilunar valves close so that you don't have your back flow remember very close and for a minute you have what's called a dicrotic notch the brief increase in aortic pressure that occurs when you pump all that blood into the aorta the aorta expands that's when you get your systolic pressure and that that process is called the dichroic notch okay total cardiac sign 0.8 seconds roughly that's a normal 70 beats per minute cystos 0.1 ventricular left atrial systole ventricular systole is 0.3 creation period which is the time in between is about 0.4 so it's right and when you that silent part that's the quietion period right overview of heart sounds the 12-point question going here remember everything that i go over is fair game i could ask you a multiple choice whatever but the written one is just from here to here and you see i know i'm sorry here here to here b one two three i know you want your stuff um yeah it'll be can you come back like at about 11 30 because i'm really busy all right heart sounds another possible uh written question and it's very easy what does the love mean what does the dog mean what does it mean yeah i'll get you a lot of points put that see what you get put that on the test let's see what happens yeah love dub it means your heart's beating okay love is a first heart sound it occurs when what happens when the av valves close that's the sound you hear from the closing of the av valve that is marking ventricular systole because you close the av valves remember i told you that's the first step for the iso volumetric contraction stage right so to start systole you're going to have to uh close the av valve so it doesn't go back where it came from and then that's a love in the dub the dub is the closing of the semi-lunar valve it's the onset of daiso because at this point you pump the blood out and so the blood is already out of um the ventricles and you don't want it to go back in so you have to close the semilunar valve to prevent that to prevent it from going back so dub is the closure of the semilunar valve the onset of ventricular diastole while love is closing of the av valve's onset of ventricular systole that's a pretty easy explanation like six points oh come on don't be greedy i'll be like four points maybe am i going to ask that yes that's what i'm telling you maybe yes well yeah so i'm gonna love duck so to get the four points what will you have to say the love is caused by av valve's closing what does it signify the onset of ventricular systole well the dub is you know closing a semilunar valve marthan said a ventricular i didn't put ventricular because i said it out loud but you'd have to put ventricular diastole because there's also atrial diastole so don't forget well i mean that's that's a summary but you'd want to put love is the sound that occurs because of closing of the av i tell you these notes are not meant to be like they're things so so you'd put the love is the first heart sound caused by the closing of the av valves and it signifies or marks the onset of ventricular systole then you would say the dub is a second sound caused by the closing of the semi-lunar valves that signifies the beginning of ventricular diastole okay if you just put closing of azure valve then i don't know that's a sound no these are just where well that that's the pause just signify this is heart sound so i asked about love and done the pause is another part of the heart done that pause is the mark of the quieting period so i could ask all these the tricuspid valve is best heard from the right fifth intercostal those are other details that right that's so hard all right um remember we already talked about that in uh lab right a murmur in fact we even had a question about that already murmur is irregular heart sound so instead of just lub dub lub dub dub you could hear or remember i told you that could mean an incompetent or stenotic valve and the reason for that is if the valve doesn't close properly you have gurgling or back flow and that's where you get the sound that's where you come with the murmur murmurs name and then sonatic valve they kind of stay open and narrow so just like when air is being forced through a narrow opening the fluid being forced through a narrow opening causes that sound sometimes you hear your pipes do that too actually if you turn on your pipes sometimes you may hear a high-pitched sound does it never happen to some people as it goes through oh you you've been here yeah that's so you already know about that cardiac output do you already know about that yes we learned it in circulation that's just a review now why did i review this cardiac output stroke volume times heart rate uh the reason is because i'm going to tell you the components of stroke volume how do you determine what stroke volume is remember stroke volume is the amount of blood that's ejected from the heart with each beat now how the heck am i going to do that well it's hard to see how much blood is actually leaving but you can see how much blood you started with how much blood you're left with after you're done and subtract the two to figure out how much blood is leaving and that's what they do they they can uh you know use radio labels right and take x-rays kind of like you know angiograms take x-rays and you can actually see what your starting volume is they can calculate it and what your ending volume is and then your stroke volume would be the difference between the two so if i start with this amount and i'm left with this amount then the difference is the stroke volume how much left so what you're starting with is called the end diastolic volume what you are what's remaining after the beat is called the end systolic volume okay when you subtract the two you get the stroke volume now what affects end diastolic volume well how much time you have to fill obviously the longer you have to fill the more blood will come in so if you don't have enough time to fill less blood will come in what determines and also venus pressure actually because the more pressure in your veins vein is the driving force for it to to fill up too so venous pressure and also the time of diastole and systolic volume what controls that well basically the force of contraction how how forcefully you're ejecting and also the pressure because remember it's the pressure difference between the aorta and the ventricles which drives it forward if i have too high pressure here less blood is going to want to go out i'm going to left with with more blood in the heart that's why high blood pressure gives you more resistance and your heart has to work harder to overcome that that's why if you have hypertension as a problem there's also something called a frank starling law of the heart basically what that says is i i like to summarize it as a rubber band rule it means the the more you stretch the heart the stronger the contraction so the primary force of the primary thing that controls contraction is how much you're stretching it just like a rubber band if i go like this the rubber band you'll bounce but if i go like this it'll bounce even more right the more i stretch the rubber band the more it'll snap back together right well same with the heart the more i fill it up the more it wants to come back kind of like a rubber band and that that is described as the frank starling law of the heart that the critical factor for stroke volume which is how much blood is detected is actually the degree of stretch of the cardiac muscle stress cells or how how how much you're filling up so increase edv equals more contraction force that's why somebody that's an athlete and even though they have a low heart rate they still have good stroke volume because their low heart rate gives them more time to fill and plus they have good circulation so they're going to have good venous pressure so it's going to fill up properly and then they can still have a good ejection phase right so exercise equals more venous blood return more time to fill so you have slower heart rate and more venous return when you are in good cardiovascular shape that's why athletes have lower than normal heart rate and they still have efficient circulation autonomic regulation of heart rates of course we know sympathetic and parasympathetic can speed up or slow down we just talked about that the sympathetic uses what norepinephrine that increases heart rate but it does maintain stroke volume and so that way you'll increase the cardiac output parasympathetic will decrease the heart rate vagal tone that's the parasympathetic inhibition allowing normal heart rate remember i told you under normal conditions the parasympathetic is going down your heart remember that's why when we put um the atropine uh the heart of the frog sped up more than just when we put the pillow carpine remember from lab we put the pillow carbine and and uh we got a slow down of the heart but then when we put the atropine which blocks parasympathetic we got an even higher than normal and that's because under normal conditions your heart is being blocked by the what parasympathetic and that's called bagel tone baro receptors and pressure receptors monitor changes in blood pressure and allows reflexive activity with the autonomics so remember you have to coordinate your supply and demand and partially your autonomics gets its information via these steroid pressure receptors can we also regulate heart rate using hormonal signals of course epinephrine epinephrine is sympathetic right it's adrenaline remember epinephrine is adrenaline and it'll speed up your heart rate thereby increasing your blood pressure yes not exactly well a bare receptor measures pressure and the pressure receptors measures pressure as well but one is the bare receptor measures like pressure of the fluid the pressure receptor is kind of measuring mechanical deviation in other cells they're both measuring pressure but it's like two different two different mechanisms for it okay but barrow receptors are pressure receptors and so are pressure acceptance it's just that one is uh used basically for fluids and that's the barrel receptors and the plasma receptors is pressure like pacinian corpuscles or something like that like if you talk about a pacinian corpuscle that would be a pressure receptor right but you don't consider that a baroreceptor that would be like a pressor receptor versus a baroreceptor would be like in the veins and arteries to detect the stretch of that you get the difference they're both measuring pressure but one is different thyroxine the hormone released by the thyroid and increases heart rate in large quantities it also amplifies the effect of epinephrine uh calcium levels potassium and sodium levels are very important obviously sodium calcium potassium all of these mechanisms there involve these ions so obviously if you mess with the levels of those you are going to have problems okay hyperkalemia increase potassium level potassium chloride can actually stop your heart remember what does that do you'll prevent the repolarization phase so you'll be stuck depolarized remember if you can't reset you'll never get the next event and so that stops the heart uh hypokalemia lower potassium levels leads to abnormal heart rate because hypocalcemia depressive heart function hypercalcemia increases contraction phase hypernatremia and high sodium concentration can block sodium transport and muscle contraction so you have all of these ionic imbalances can cause you to have problems other factors affecting heart rate normal heart rate of course the little baby has the highest because of course they have high demand so they need a high supply female 72 to 80 males 64 to 72 now generally the males have higher but in terms of the beats they have they have more red blood cells and so they generally have more muscle mass so they have more venous return and so the heart rate is actually slower generally of course mine is probably 120 but out of shape all right although my dad before he died when he first started going he had a resting heart rate of almost 300 that's when he first went to the hospital i mean he couldn't even stand or walk i mean doing nothing he had severe atrial fibrillation and his heart had gotten so enlarged and saying that he wasn't doing anything and it was like almost 300 it was it was crazy that was his resting heart rate and so of course you have to take medication blah blah blah damage your liver long story short well different things i mean of course those genetic predispositions and uh you know environmental damage i mean he grew up in a third world country in an orphanage and you know who knows what damage he he sustained over his lifetime and uh you know for whatever reason his heart was inefficient he didn't know about it and so years of inefficiency caused this progressive build build up and then it was too late all right that's the tachycardia uh bradycardia is lower than normal heart rate symptoms physical conditioning can actually cause it but it's a sign of pathology if you're not healthy so if you're healthy of course that's a good thing but if you're not healthy then that means that your heart won't be able to distribute properly imbalance of cardiac output congestive heart failure heart cannot pump sufficiently sufficiently to meet the needs of the body so you get a backup so if your heart can't pump sufficiently then you get a backup if you can't pump if if your right heart going to your lungs can't come properly you get a build up in your body if the left part of your heart which pumps to the rest of your body has a backup you get a build up in your lungs okay that's why they call it congestive heart failure because you get a build up of this fluid because your heart is inefficient coronary artery sclerosis leads to gradual occlusion to hard vessels reduces oxygen nutrients supply to cardiac muscle cells risk factors include a fat and salty diet smoking stress high blood pressure when aortic pressure gets too large that ventricle cannot compar properly increasing esv which is the what end systolic volume and lowering the stroke volume myocardial infarction that's a heart attack right heart cell death pulmonary congestion is a failure of the left heart i just told you that peripheral congestion all right heart pathologies congenital heart defects heart problems that are present at the time of birth this is just one example of a congenital heart defect patent ductus arterosis when you're a fetus you have shortcuts throughout the circulation because obviously you're not breathing air so you have a lot of shortcuts like for instance you have the foramino valley that's between the two atria you also have the ductus arterosis right you have these shortcuts because you want blood to go through your lungs but you're not really getting oxygen from there because the blood is already oxygenated by the mother so you have these shortcuts that help circulation but they have to close up when you're an adult and you well not an adult when you are born so that when you breathe air you won't be inefficient because you don't want to mix low oxygen with high oxygen you want to be separated to maximize the intake okay so that is one example of a congenital heart defect sclerosis of av valve and i think maybe like with my dad it may have been congenial because he said that all his friends when he was young were playing soccer and he would get tired while nobody you know they wouldn't and so he think you know maybe it started as some sort of congenital heart defect that like built up over the years sclerosis of av valves fatty deposits on the vowels particularly the mitral valve of the left side it leads to heart murmur okay uh declining cardiac reserve heart efficiency decreases with age sorry to say no matter what as you get older your heart starts to decline but that doesn't mean that exercise does you no good there are 90 year olds that run a marathon i can't run a marathon but if that 90 year old started running marathons in their 20 of course in their 20s they would have better time than in their 90s that doesn't mean a 90 year old can't be better than a 20 something year old if the 90 year old you know works out and a 20 year old doesn't but if you are a professional athlete and you work out in your entire life when you're younger you'd have better times than when you're older period okay but that doesn't mean you can't slow the decline and you still can't get benefit so no matter how old you are you should start exercising and keeping well because even though you are decreasing with age no matter what you all are i am yeah which is funny because when i was a kid i did run a couple and then uh you know as i got older i'm like why did i do that what's the point you know so at this point i would probably never run a marathon again yeah all right anyway fibrosis and conduction problems nodes and conduction fibers become scarred over time may lead to arrhythmias so these are just some problems all right moving on now respiration is long so