hello and welcome to another episode of study this where we review various textbook chapters today we'll be going over chapter 9 of chitin and halls mythical physiology which goes over the hearts anatomy and the heart muscle and how it functions as a pump in order to move blood around the body the heart can be thought of as almost a mechanical pump in association with a electrical circuit and we'll go through the pretty basic components of the heart during this chapter if you're feeling generous please feel free to give the video a like and subscribe it will help the channel out so we start off by describing the actual anatomy of the heart we do have a picture here are they a heart I hopefully we know our different chambers but just a quick revision we have the top chambers which are the atrium so this is the right atrium on this side this is the left atrium which empty blood into the muscular chambers called the ventricles which then propel that blood either to the lungs through the pulmonary artery or through to the body through the aorta and we have three types of muscle fibers here we've got the atrial muscle we have the ventricular muscle and then we have our conductive muscle fibers the conductive muscle fibers are technically muscle fibers but they do not function to contract and propel blood they function to propel electrical signals around the heart to tell the heart to pump in a synchronized matter so to start with the cardiac muscle itself is striated and it's organized to what's called a syncytium which is best described over here where we have our cardiac muscle cells and you can see that they're organized in parallel and in series with one another where each muscle cell is attached to another one and they're attached by these intercalated discs and this allows the ions within the extracellular fluid to flow freely between them and if a heart muscle is contracting that contraction will then propagate through to the other muscle cells so we have two types of systems here we've got the atrial and then also the ventricular so that atrial muscle will all contract as one and then the ventricular muscle will contract as one and the atrium and the ventricle is actually divided or separated by a fibrous layer so there's action potentials we've already we talked about in a previous chapter on action potentials if you can remember this action potential different from our standard ones because there is this plateau and this plateau to our action potential occurs because of calcium channels and these calcium channels which we call the l-type calcium channels they will open to allow an influx of calcium into the cell pro longing this depolarization period because we have an influx of positive ions keeping the membrane potential within the cell as positive so we have four different phases we have phase zero and this is our normal sodium channels opening to allow an influx of sodium and an influx of positive ions resulting in a sharp increase in our membrane potential those sodium channels then close and there is a small rush of potassium ions leaving the cell which results in this little dub but then there is a reduced permeability to those potassium ions and then the calcium channels open the l-type calcium channels so then this allows calcium to diffuse into the cell for a prolonged period of time allowing the heart to contract at the same time so this prolonged action potential occurs in our contraction can also occur in a prolonged manner and then once those calcium channels closed our potassium channels open allowing an e flux of potassium out of the cell repolarizing it resulting in our standard resting membrane potential and that's also described here with this little diagram where we have that short spike of sodium we have that prolonged plateau of calcium and then a reduced permeability to our potassium ions resulting in this plateaued action potential and then another factor to consider is our refractory periods so we do have a period in which an action potential will not be able to be propagated so once the action potential occurs we cannot obviously have another action potential at the same time and we have to wait for repolarization to occur and repolarization there is a short little segment which technically is still within the refractory period as our ions are storm risk blushing themselves however once we get close to normal there is this relative refractory period where a stronger than normal stimulus may be of the result in the early action potential and an early contraction which would be called a premature contraction or premature eat so then we get into how the action potential actually causes a contraction and this occurs through the excitation contraction coupling that we have briefly talked about before we will get into more details in this chapter and we can describe it all using this diagram here where we have an action potential there spreads across the membrane resulting in an influx of calcium ions travels down our T tube you which is a lot larger and our cardiac muscle compared to our skeletal muscle and actually contains a lot of negative mucopolysaccharides on the membrane which actually helps to store some extracellular calcium and then that extra calcium is able to diffuse into the cell during our action potential which does initiate opening of the ryanodine receptors on the sarcoplasmic reticulum so there is even further influx of calcium into the cell however the SR is not as well established in cardiac muscles compared to skeletal muscle so the predominant calcium entering the cell is actually from the extracellular fluid and the cardiac muscle is actually very dependent on the extracellular fluid for its contraction so once that calcium enters into the cell we then get our contraction of actin and myosin just as we've talked about in the skeletal muscle contraction chapter all are associated with those cross bridges forming and then the walk along theory once contraction has occurred and we want relaxation to occur we have to get rid of all this extra calcium so calcium is not only pumped back into the sarcoplasmic reticulum but it is also actively excreted out of the cell using the sodium calcium counter transporter and that occurs because there is a higher concentration of sodium in our extracellular fluid so passively wants to diffuse into the cell but even gets pumped straight back out by the sodium potassium ATPase so that passive diffusion of sodium into the cell allows calcium to leave the cell and then that allows the muscle to relax so cardiac cycling essentially just means an entire heartbeat or the entire cycle sinus node all the way through to atrial and ventricular contraction all the way to ventricular relaxation and when the heart rate increases we have a reduction in our cardiac cycle so systole which is contraction reduces as well as diastole which is relaxation however the portion of reduction is greatest in diestl II so if you have a reduction and cardiac cycle due to an increasing heart rate you actually further reduce the period of diastole so you fill with less blood with a faster heart rate and systole does reduce but not to a greater extent and the entire cardiac cycle can be explained quite thoroughly using the wiggers diagram which has several components within that so that includes a phono cardiogram which is recording the actual heart sounds that you can hear so a loved and then a dub and then there is two other heart beats that you can occasionally hear which I depicted here and will also be here which isn't depicted in this diagram so we have four heart sounds but we typically only hear the two we have an electrocardiogram showing our electrical activity of the heart so a P wave QRS complex in our T wave we've got volume so volume increasing and reducing as with our heart is beating or systole is occurring and they're refilling during diastole and then we have relative pressures so we've got the ventricular pressure in the red atrial pressure this dotted line down the bottom and then a water pressure at the top here so if we briefly go through each component we have a p-wave which constitutes the sinus node firing and then movement of electrical activity through the atria we then have a slight increase in atrial pressure as that pushes more volume into the ventricle and then once the ventricle has been filled with fluid there is a brief delay due to the AV node atrioventricular node giving time for that ventricle to fill with blood and then that the signal is sent through the ventricles and that's correlates to our QRS complex which is the electrical signal seen getting sent through our ventricle so then there's always a slight delay between electrical activity and mechanical activity because electricity moves faster and then it signals the muscle to contract so the contraction period is this entire period here and we are getting an increase in pressure as the hearts contracting as the ventricles contract and then our volumes reducing and then once the pressure within the ventricle reaches the same pressure as the a order in the Eldar valve will open allowing that blood to be ejected out of the heart once the ejection occurs we see the reduction in ventricular volume until contraction as over our systole is over and then the heart starts to relax and the pressure reduces and at this time the aortic valves closed to stop blood from rushing back into the heart and we get a relaxation period where there's no filling of blood until the atrioventricular valves open because the ventricular chamber now reaches the same pressures of atrial chamber so then that AV valve opens blood is now able to rush into the ventricle during diastole until the next atrial contraction occurs pushing that little extra blood and there's another QRS complex resulting in increased pressure within the ventricle and taller breaches are other pressures opening that will look Val ejection of blood and then relaxation occurs aeolic valves closed and we have relaxation without filling until we reach the same pressure as a atrial pressure and then atrioventricular valves open allowing diastole and filling of blood so that is the entire cardiac cycle and we do have several components that we should briefly talk about and this include some definitions so we have systole the period of ejection diastolic the period of filling we have isovolumic relaxation time which is that time that the heart is relaxing and there's no filling of blood anyway isovolumic contraction time where the heart is contracting but there's no blood leaving the ventricle because we haven't overcome that aeolic pressures yet and we haven't opened up the Outlook valve so that's isovolumic contraction then we have isovolumic relaxation and then we have systole and diastole there is also three phases to diastole or the filling of the heart with blood and the first phase is when those atrioventricular valves open as the atrial pressures overcome the ventricular pressures as they're relaxing that opens up the atrioventricular valves and there is a rush of blood from the atrium into the ventricle then there's the second phase where there is passive filling of the ventricle as blood is draining from the rest of the body through the veins into the atrium and straight through into the atrioventricular valves and then there's the third phase which is occurring with the excitation of the atrial tissue and contraction of the atrium resulting in active filling stellarium pushes the extra little blood into the ventricles so then the ventricles should be nice and full ready to eject that blood around the body now we've briefly talked about these two valves in the heart these two types of valves with the atrioventricular valves which are quite flimsy or not as robust because they don't require much pressure for them to close because the ventricles going to start to contract and then as the pressure in the ventricle quickly raises above the pressure within the atrium these AV valves are going to close and they're also attached to this chordae tendineae t2 papillary muscles which contract at the same time as the ventricles closing to hold the valve from being prolapsed into the atrial chamber and then we have our semilunar valves so our other can pulmonic valves and they're located just at the entrance to the a order or the pulmonary artery and then we'll robust because they're dealing with much higher pressures from the blood that has just been ejected from the body and wants to rush back into the heart once the heart starts to relax so those are our two types of valves atrioventricular valves separating the atrium and the ventricle and then our semilunar valves which is stopping blood from flowing back into the heart after it's been injected and the entire contraction relaxation process we've talked about has been modeled in this volume pressure diagram so you can see here we have volume at the bottom pressure at the top and this is recorded by floating a catheter within the ventricle and then just recording the volume within the ventricle at the same time as the pressure so this first phase here is representing diastole or relaxation as volume is increasing without much increase in pressure phase two is isovolumic contraction so that's contraction of the heart muscle without ejection of blood and you can see that the volume is staying the same and pressure is rising and once we overcome that a order pressures or the pulmonary artery pressures on the right side then we actually have the period of ejection so phase three until we've pushed all that blood out and we want to relax and then we have a period of the isovolumic relaxation where we're relaxing without any filling from the atrium because those AV valves are still closed until the ventricular pressures are lower than the atrial pressures and those atrioventricular valves open allowing gaya study to occur and these loops will follow the blue line and the green line here where if there is an increase in diastolic volume you will have a steady increase in pressure to a point where it becomes exponential because there is a fibrous membrane around the heart called the pericardium which means that the heart can't continue to expand as much as it wants so once we hit the limits and the pericardium starts to restrict the increase in the heart size we get a dramatic increase in in diastolic pressure with small increases in volume on the other side which is systolic pressure increasing volume will increase systolic pressure due to the frank-starling mechanism and we will talk about that very shortly so an increased volume stimulates an increased in systolic pressure or contraction up to a point so once we reach this peak and we start to go down to an increased volume results in reduced systolic pressure that occurs because those actin and myosin filaments and no longer optimally alliance so they are being pulled apart by the exists of volume and we can't get an increased in contraction and so this diagram is able to quite nicely illustrate our changes and volume and how that relates to pressure within the heart and this is just a blown-up version of that volume pressure diagram that we've already talked about so we have these four turning points so at the onset of diastole we have the opening of the mitral valve in the case of the left ventricle once contraction occurs mitral valve closes and contraction is isovolumic until the aortic valves open allowing ejection and in the air the valves closed allowing relaxation without filling in this period from end diastolic volume to in systolic volume is our stroke volume - how much volume of blood was ejected out of the heart and in the area under these arrows is called the external work so how much work the heart is are actually under doing all the kulluk output of the heart and then that really covers the main components of that diagram so we can briefly talk about now how an increase in volume actually results in an increase in contraction and as related to the frank-starling mechanism where the increased volume has been found to just result in an increased contraction so that's one component of it but then also an increased volume or stretch within the atrium actually stimulates a faster heartbeat so we actually get a faster heartbeat in addition to a more forceful contraction and since cardiac output is heart rates times stroke volume which could be thought of as contraction then we get an increased cardiac output in a response and then we have different mechanisms by which the heart can speed up or slow down and we'll start off by talking about the autonomic nervous system so as you'll see here we have the parasympathetic and sympathetic nervous system which innervates into the heart the parasympathetic nervous system which comes by the vagus nerve innervates mainly onto the sinoatrial node and the atrioventricular node in parasympathetic stimulation results in depression of heart activity and that depression of heart activity since we're innovating mainly at the nodes results in a reduction in heart rate there is a very small reduction in contractility but this mainly reduces heart rate where is sympathetic innovation you'll see is innervated and essentially all the parts of the heart so when the sympathetic nervous system is stimulated through the fight-or-flight then you will actually have an increase in heart rate and also an increase in contraction so we get a larger response and a cardiac output as you can see here from Figure 9-14 without any stimulation we have a cardiac output which is the green line here with parasympathetic stimulation we have reduction in cardiac output with maximum sympathetic stimulation we get a dramatic increase in cardiac or because of that increase in contractility at the same time potassium ions and calcium ions and the extracellular fluid compartments can also affect the heart potassium ions essentially result in a dilated flaccid heart because of blocks conduction of the electrical signals so you have a reduction in heart rate and also a reduction and contractility because your resting membrane potential has become less negative so now there's less of a driving force for the action potential to no stimulate a strong heartbeat calcium ions if you have too much calcium then you get the opposite of too much potassium so you get contraction because as you'll expect with calcium being the main driver of cardiac muscle contraction you're going to have essentially an irritated heart whereas if you have the other side where you have a deficiency of calcium ions which you get weakness of the heart so that's what calcium is so important to the heart muscle temperature can also affect the heart rate where an increased temperature results in a faster heart rate up to a point we start to actually use too much metabolic reserves and you can actually result in weakness and in arterial pressure where arterial pressure actually has very minimal impact on cardiac output now our terrible pressure is increasing what's called afterload so that pressure that the heart has to overcome to eject blood out of the heart you would expect an increase in arterial pressure to result in a reduction and cardiac output just because it has to keep pushing harder and harder against a greater pressure out in the arterial system however the heart's cardiac output actually stays relatively the same during a normal arterial pressure up to a point and then up to about 160 millimeters of mercury mean arterial pressure once we overcome that cardiac out what does reduce because that is just too great of a pressure for that heart to overcome and that really summarizes the end of our chapter there and I hope you enjoy that feel free to drop a comment otherwise we'll see you in the next chapter