hey guys it's medicosa's perfect snail is where medicine makes perfect sense welcome back to another cardiophysiology video in my Cardiology playlist hey guys it's medicosa's perfect snail is where medicine makes perfect sense welcome back to another cardio physiology course your heart is like a factory there is an input going into the heart and there is output leaving the heart the input is via veins whereas the output is through arteries any Factory that has an output can measure that output roughly speaking by multiplying the number of employees times the productivity per employee similarly you can calculate the cardiac output by multiplying how fast the heart is pumping I.E beats per minute times the volume ejected per beat I was not planning on making this video however a wonderful person named Jordan supported me generously and said hey medicosis would you please create a cardiophysiology video my dear Jordan of course I can and your support means the world to me so if you're watching this video right now please take a moment and say thank you to Jordan in the comments section let's put a smile on his face today and if anyone wants me to create a specific video on a specific topic you can do so on my website in today's lecture we'll talk about the cardiac output the cardiac index heart rate and stroke volume we'll talk about the end diastolic volume and systolic volume ejection fraction startling law versus Sterling forces talk about compliance which is the opposite of elasticity we'll talk about the cardiac cycle and the dreaded most hated pressure volume Loop for some reason students hate this but it's actually a piece of cake if you understand it properly this video builds upon previous videos in my biology playlist and in my Cardiology playlist such as the cardiovascular system video and my video on the cardiac cycle and blood pressure here's your wonderful heart how many hearts do you have anatomically one physiologically two there is the right heart and there is the left heart let's start here left ventricle pumps blood to the aorta this is oxygenated blood the aorta distributes this oxygenated blood to every organ in your body each cell takes in oxygen and nutrients from the arterial site and dishes out carbon dioxide and waste into the venous side the venous side will go here in few Villages right atrium right ventricle passing through the tricuspid valve by the way every valve in your heart has three cusps except this one this one between the left atrium and the left ventricle has only two cusps it's the mitral valve why do they call it mitral because it's similar to lamita which is a religious head for some Catholic clergyman back to the deoxygenated blood in the right ventricle it will be pumped through the pulmonic valve into the pulmonary artery and then it will take me to the lungs the lungs will get rid of that carbon dioxide through exhalation and then inhale some oxygen all of that oxygenated blood will go to the left atrium via pulmonary veins then oxygenated blood enters left atrium and then through the mitral valve we go to the left ventricle and then you repeat the story again what's the next valve here aortic valve the basic idea is that your heart is a factory there is input to that factory there is output from that Factory and then you distribute the widgets the input to the heart comes through veins if you are the right heart it comes through the superior and inferior vena cava if you are the left heart it came through the pulmonary veins so input is Venous let's talk about output if you are the right ventricle your output will go through the pulmonary veins if you are the left ventricle your output will go through the aorta so the output is arterial then then these arteries will distribute that oxygenated blood to every organ in your body input is Venous output is arterial let's forget the distinction between the right heart and the left heart for a second and let's just imagine it's one chamber there is input coming to that chamber and there is output leaving the chamber the output leaving the chamber is going to are trees and therefore is going to be responsible for arterial blood pressure how do I measure the output of that factory you need the number of employees working in the factory times the productivity per employee how many times the heart is pumping per minute is called the heart rate beats per minute times the volume ejected per beat how fast times how strong the heart is beating equals the output of the heart in every minute heart rate is measured in beats per minute stroke volume is measured in and ml or volume per bait and then the bait will cancel with the beat and you end up with ML on top minute at the bottom this is the measuring unit for the cardiac output which is about 5 liters per minute or 5000 ml per minute so hey medicosis how much does my left ventricle pump per minute 5 liters per minute how about my right ventricle then also 5 liters per minute and what's the average volume of the adult blood it's about 5 liters so you're trying to say that my blood circulates throughout the entire body once every minute that's true and your heart has been doing this every minute in every hour in every day and every week and every month and every year that you've been alive look these numbers are just approximations to make the calculation easy so that 100 times 50 equals 1000 ml per minute in real life if you want to be more accurate this is more like 70 and this is more akin to 7th a pearl for the prose do you know the equation of the cardiac output is exactly the same as the equation of what minute ventilation for the lungs which is the ventilation of my lungs per minute how much is that well how fast is the long breathing it's called the respiratory rate times how much air do I get in per breath and this is called the tidal volume when you multiply the tidal volume times respiratory rate you get the minute ventilation which is equivalent to the cardiac output it's the same exact concept how fast times how strong medicine makes so much sense once you understand what the flip you're talking about why should I care about this because during pregnancy the volume of plasma goes up which means the volume of blood goes up which means there is more input of blood coming to Mommy's heart which means the output has to be higher when the Venus return that's returning to the heart goes up the stroke volume goes up which means the cardiac output goes up moreover in pregnancy the heart rate also usually goes up so in a nutshell pregnancy has high cardiac output which makes sense because Mommy now has to support herself and the baby now is it fair to compare the cardiac output of a tiny person like medicosis with someone huge like Michael Jordan LeBron James the rock or whomever no it's not fair if you compare my heart to his heart he will be under the impression that I have a heart failure because my heart sucks compared to his so what should we do well let's make it fair let's divide the cardiac output per body surface area you divide myocardic output by my body surface area and his big cardiac output over his big body surface area and when you do this you will realize that my heart is normal and I do not have heart failure and this is called the cardiac index ml per minute is for cardiac outputs square meters is the measuring unit for the surface area therefore 4 here is the measuring unit of the cardiac Index this cardiac output is important because who's going to depend on the cardiac output your blood pressure I mean the mean average systemic notulmonic arterial in the systemic arteries like the radial artery blood pressure pressure of blood in these systemic arteries averaged and this equals cardiac output which equals what heart rate time stroke volume multiplied by the total peripheral resistance which depends on the radius to keep it nice and easy think of the resistance as the opposite of radius but it's not any radius its radius raised to the fourth power the lower the radius the greater the resistance if the radius decreased to half of its original value do you know what's going to happen to the resistance please do not say it's going to double H2 power 4. I.E the resistance will increase and go up it will become 16 times greater than the original value so vasoconstriction decreases the radius increases the resistance which increases the total peripheral resistance which means the blood pressure will go up conversely vasodilation increases the radius lowers the resistance and lowers my blood pressure the input is Venous the output is arterial the cardiac output affects my arterial blood pressure because blood pressure equals cardiac output times tpr the input is Venous right so we can call that input venous return and when the heart is receiving blood the heart will relax diastole so the volume of blood in the heart at the end of diastere is the end diastolic volume which equals the venous return which equals the pre-load which is the load given to the heart pre before the heart contracts then what would you call the load a put upon the heart after it contracts after load and it will be arterial afterload is arterial next many students struggle with the concept of ejection fraction and diastolic and systolic and all of this nonsense it's a piece of cake look imagine that I gave you 10 apples you decided to keep four apples for you and eject or give away six apples let me ask you a question how many apples did you eject answer six what's the volume of apples that you ejected six apples the volume that you ejected is your stroke volume so the stroke volume is six apples the four apples that you decided to keep is the end systolic volume which is the volume remaining in the heart at the end of systole I.E it didn't leave the Heart during contraction so when I came at the end of systole after the heart has finished contraction I found for app is still with you that you did not eject and what do you call the 10 original apples that I gave you and diastolic volume because at the end of diastere you just relax and accepted all the apples you had 10. 10 is the end diastolic volume 4 is the end systolic volume the difference between them is the stroke volume so stroke volume equals end diastolic volume minus end systolic volume okay if I gave you 10 apples a new ejected six what's the percentage that you ejected of course it's going to be 60 percent that's right and we call this the ejection fraction but hey maticosis let me ask you a question did I eject six apples or did I eject 60 percent well if you're talking in absolute terms the answer is six apples but if you're talking in relative terms it is 60 percent the stroke volume is six because the stroke volume is the difference between the two the ejection fraction is this stroke volume that you ejected over what I gave you in the beginning so it's the stroke volume over the end diastolic volume and since we know that the stroke volume is 80 DV minus ESV we can also say that the ejection fraction is ADV minus ESV which is the stroke volume over 80v what you ejected over what I gave you in the beginning absolute terms versus relative terms so if the heart receives more input I.E more preload which means more venous return which means more end diastolic volume of course the stroke volume will increase if I gave you 20 apples instead of 10 of course you can eject more assuming that you will still eject sixty percent sixty percent times 20 is greater than 60 times 10 which means that your cardiac output goes up because cardiac output equals stroke volume times heart rate so if the stroke volume goes up cardiac output goes up and when cardiac output goes up arterial blood pressure goes up what are the factors that affect myocardiac output then well preload affects the cardiac output after load affects the cardiac output einotropy or the force of contraction of the heart affects the cardiac output as well as the heart rate let's talk about that remember please that preload is Venus but the afterload is arterial hey preload I mean Venus return I mean end diastolic volume I mean the input to the heart if you go up of course more input equals more output let's dig deeper more input equals more stroke volume equals more cardiac output what are the factors that will increase the input I.E the preload I.E the venous return I.E the edv of the heart how about if I have more blood like in pregnancy or if the doctor gave me too much fluids this will raise the preload which will increase the cardiac output how about increasing my venous tone Oh if your veins constrict they will be able to force more blood from your ankles to your heart upwards they are squeezing themselves more more input equals more output what if I increase the skeletal muscle pumping action let's talk about for the skeletal muscles over your leg the reason your blood is capable of going up against gravity is number one that the veins have valves number two is that your skeletal muscles in your legs contract and force the blood to go up and not down third you have negative endrathoracic pressure in your pleural cavity the more negative this pressure becometh up here the more you suck blood upwards which means the greater the venous return which means higher preload and higher cardiac output How about if this Atrium contracted more then you will push more blood to the ventricle which means you're increasing the ventricular end diastolic volume which means you're increasing the stroke volume which means you will increase the cardiac output let's talk about the opposite the factors that can decrease the venous return or decrease the edv what if I have pericardial effusion or Worse cardiac tamponade accumulation of fluid or blood around the heart or what if my pericardium is calcified as hard as a rock constrictive pericarditis do you think my heart will be able to relax and accept all of that blood input no my heart will not be able to accept all of that blood therefore what's going to happen preload will go down cardiac output will go down similarly if my ventricle not the pericardium per se but the ventricle itself is very stiff as in restrictive cardiomyopathy which could be caused by sarcoid amyloid hemochromatosis cancer and fibrosis do you think my heart will be able to relax and receive all of their input no no input equals less cardiac output next how does the afterload which is arterial affects myocardic output think about it increased after load could happen because my arteries are constricting when you constrict something you increase the resistance which increases the pressure in the arteries now put yourself in the shoes of the left venture is it easier or harder for you to pump blood when the arteries in front of you are constricted of course it will get harder therefore what's going to happen to the volume that you will eject it will get lower which means the cardiac output will go down and when you pump less blood and I look inside that ventricle after systole at the end of systole what will be the volume oh more blood will stay here because less blood was ejected instead of ejecting six apples I ejected three what's gonna happen well seven will remain inside instead of four which means the ESV went up and when the ESV goes up what's going to happen to the stroke volume which is the difference between ADV and ESV of course it will decrease next the effect of force of contraction contractility inotropy on the cardiac output of course the stronger I contract the greater the output because if you contract harder you will eject seven apples instead of six seventy percent instead of sixty percent leaving less apples left after the contraction I.E lower ESV which means the stroke volume is higher because the ejected seven Apple's ejection fraction is higher cardiac output is higher next heart rate be very careful here under physiological conditions if your heart rate increases a little your cardiac output increases a little however don't forget that your body has some Regulatory and compensatory mechanisms which means your body can adjust the venous return So at the end of the day no significant change the cardiac output will happen however if your heart rate increases a lot and I mean crazy fast and instead of 90 beats per minute your heart is beating 220 beats per minute this craziness will give us less time to fill the heart with blood I.E less input which means less output even though the heart rate goes upper like this and the heart rate time stroke volume is calling carbon yeah because because when you do this there is no time for you to fail it takes time to fill the heart with blood this crazy fast heart rate gives us less time available to fill the hearts of the cardiac output decreases and of course it makes sense that if I'm sleeping low heart rate low stroke volume low cardiac output quiz time oven became pregnant before pregnancy she was here here is my right itch of pressure and here is my Venus return what do you think is going to happen when she becometh pregnant so let's talk about that here is the Baseline the original point is here if I go to point 1 it means that the right HL pressure goes down but there is no change in the Venus return on the y-axis how about 0.2 it means that the right atrial pressure went up and there is no change in the Venus return 0.3 is decrease in both right atrial pressure and venous return 0.4 is increase in both because the x-axis and the y-axis are increasing as for 0.5 it's only an increase in the venous return When no changes happening in the right atrial pressure so what do you think actually happens during pregnancy there is increased plasma volume and when the plasma volume goes up what's going to happen I'll have increased venous return and when the Venus is returning more blood to the right atrium what's going to happen to my right atrial pressure it will also go up so the answer is 4. I've told you before that pregnancy is a cause of hyperdynamic circulation I.E high output cardiac failure we will not call it cardiac failure in pregnancy because pregnancy is not a pathology it's normal so we just call it high output state or hyperdynamic circulation where everything is fast everything is dilated everything is distended input is Venous output is arterial preload is Venus after Lotus arterial next let's review what we have talked about before in my video on isometric versus isotonic contraction you will find it in my muscle physiology playlist suppose that I'm trying to pull this but I cannot pull it it's so heavy I couldn't pull it do you think my muscles are shortening no I could not I wish I could shorten my muscle contract it and pull it here I could not which means the length of my muscle stayed the same ISO means the same or equal metric means the length from meter the length of the muscle did not change I.E isometric contraction you know what did change the tension went up so an isotonic contraction isotonic the tone stays the same what changes then the length of the muscle changes it got shorter because I was capable of pulling up the weight in isometric contraction however ISO same length there is no change in the length what happened the tension went up in isotonic the tone is ISO did not change what changes is that muscle got shorter so look at this yeah the muscle got shorter I.E there is an actual change on the y-axis but in I isometric contraction the length of the muscle stay the same what increase then it's the tone it went up as you see here quiz time which situation among these three will help you throw your arrow farther please pause what do you think the answer is B of course with optimal stretch you get the best response just like your heart if the preload increases a little optimal increase the heart can accommodate this the heart will relax more and pushes more but if the preload increases too much what do you think is going to happen lower stroke volume and lower cardiac output the best point the highest point the maximum contraction happens with Optimum stretch less than that and you get less contraction more than that and you also get less stroke volume and this is called what the Starling law the greater the initial muscle fiber length I.E preload the more will be the active tension developed during its isometric contraction add infinitum no within limits if you go too far you will get the opposite result quiz time which situation among the three will help you throw your arrow farther please pause and the answer is B again y look at a there is overlap between the myosin actin they are just on top of each other that's not good stretch me more please oh look at this that's Optimum so that we have the greatest number of cross Bridges between actin and myosin but if you stress me too far look at that myosin can barely grab the actin same idea again which situation is the most Optimum the answer is B is the most optimal of course he who better understandeth muscle physiology wins in the Olympics so increase the preload might be okay for the cardiac output within limits here is my stroke volume against the end diastolic volume and here is my Baseline between graph a and graph B which one represents the effect of dobutamine on a healthy heart please pause let's talk about that what does dobutamine do dobutamine is a beta-1 Agonist when you stimulate beta 1 on the heart what do you get you increase heart rate you also increase the force of contraction which increases stroke volume both of which will increase my cardiac output so the answer is a in either case here let's take the same point from the x-axis because I'm giving you 10 apples each time and the first situation you only throw back three apples here six apples here eight apples so of course 8 apples is the high stroke volume and the highest cardiac output this is a positive enotropic drug here is my cardiac muscle cell here is my beta1 receptor and here is dobutamine stimulating the beta1 receptor beta 1 is GS coupled which means they'll activate as in late cyclase which means we'll convert ATP into cyclic amp which activates the protein kinase a which opens the calcium channel calcium enters into the cardiac muscle cell calcium induced calcium release from war from the jail of calcium the sarcoplasmic reticulum and this calcium will make actin and myosin bind to one another and boom you have contraction of course it's good to have normal preload and afterload if I've told you that you have been cursed by one of these either High preload or high afterload which one will you choose I'll choose High preload because within limits I can counteract this I can adapt to this by increasing my force of contraction however when you increase afterload well it's called afterload for a reason after the heart contracts the heart was surprised that there is too much load too much resistance in front of it due to vasoconstriction atherosclerosis hypertension Etc so the afterload is evil preload is Venus after Lotus arterial an increase in the preload is less evil than the increase in afterload when it comes to the afterload the greater the load that you add on top of the heart what's going to happen to the velocity of shortening I.E the contraction shortening of muscles it goes down it's an inverse relationship translation the greater the afterload the lower the stroke volume and vice versa after load is evil quiz time weight lifting we have two types there is the snatch and there is the clean engine which one do you think is easier please pause the answer is the clean and jerk why because I can hold this bar up here for a while and anticipate and feel its weight so that the next part is expected and therefore easier but here I have to snap match it very quickly this is like increased preload you can expect that and adapt to it and this is the increased afterload if you do not believe me go look at the Olympics records for the same player you'll find that for every player their record on the clean and jerk is higher than the record on the snatch it's all about physiology baby it's all about Starling law which is not to be confused with startling forces I.E hydrostatic pressure versus oncotic pressure hydrostatic pushes uncuttic pulls hydrostatic pressure which pushes depends on the volume of the plasma uncut pressure depends on the proteins in the plasma namely albumin because it's more numerous because osmosis cares about the number of particles and not the size osmosis is a colligative property and remember when we talked about this in your kidney here's the afferent arterial and here is the neph front if I'm pushing I'm hydrostatic if I'm pulling I'm uncortic this is true for the afferent arterial it's also true for the nephron tubules if I'm pushing hydrostatic if I'm pulling uncortic each one of these four forces can be measured in millimeters of mercury and then you give me the net filtering pressure net filtering pressure if I'm trying to move from here to here look at this Arrow which is capillary hydrostatic pressure are you with me or against me with me so it's a positive number how about you with me it's zero it's also positive here so 60 plus 0 that's on one side who are the forces that are against me you are against me because I'm trying to go this way and you're moving in the opposite direction and you are against me add them together and get the difference 60 on one side favoring forces minus 50 on the other side opposing forces the end result is a positive 10. if it's positive we're going this way if the net is negative 10 we're going the opposite way so please do not confuse stalling forces with Starling law if you want more detail about stalling forces check out my video titled starting forces in my Cardiology playlist next let's talk about compliance compliance is the same as or almost the same as expensibility or distance ability the ability to expand I.E increase your volume given a certain pressure large veins can expand expansibility compliance distensibility Big Time therefore their compliance is high relative to arteries when I constrict my vessel oh oh oh you're constricting you're pushing in it gets harder to expand so compliance goes down as I get older or as I develop worse atherosclerosis my arteries get more stiff I.E harder to expand so compliance drops what's the difference between static versus Dynamic compliance just ask yourself is the factor changing from day to day or does it take way longer than that if it's changing on day to day this is dynamic such as the degree of sympathetic activity yeah today in the morning I can have a certain sympathetic activity and then in the next minute it it changes goes up or down so that's Dynamic but age atherosclerosis oh these take a long time to change and this is called Static compliance which means that atherosclerosis and old age are decreasing which kind of compliance the static one but when the sympathetic constricts vessels that's the dynamic one compliance is the opposite of stiffness if my arteries become more stiff they become less compliant moreover compliance is the opposite of elasticity if something is more compliant it is less elastic and vice versa do you remember my language emphysema it was like Alex rubber bandsaw Very Old Sock easy to expand yeah but then when you let it go it will never recoil back because the rubber band is toast is this compliant yeah because compliance means expensibility it's very easy to expand so it's very compliant is it elastic oh heck no because it cannot recoil on its own the exact opposite is the lung with pulmonary fibrosis or restrictive lung disease the rubber band is very strong and the sock shrinks even more in the laundry washing machine is it easy to expand oh no so compliance is low is it easy to recoil the air trick it's very good at recalling because the rubber band is very strong so elasticity is High quiz time which of the following graphs represent superior vena cava is it X or Y how about which graph represents a branch of the radial artery X or Y which one is more elastic X or Y enter the superior vena cava is a big vein veins are very compliant because you can expand them big time a branch of a radial artery will be an artery or an arterial arterials are elastic stick but not compliant relative to vein so the answer is why it's easier to expand the vein than an artery at a given pressure so which one is more elastic the one that's more elastic is the one that is less compliant I.E the artery so relatively speaking veins are more compliant arteries are more elastic this is a nugget next let's talk about the cardiac cycle and the topic that everyone loves pressure volume Loops please watch the video in my biology playlist before this one left ventricle aorta the rest of the body and then Superior inferior vena cava go right atrium right ventricle pulmonary arteries lungs and back to the pulmonary veins when valves close they give us a sound when they open they give no sound the first hard sound is caused by closure of the mitral and tricuspid valve but the second hard sound is due to the closure of the aortic and the pulmonic valves which one happens first like electricity or muscle contraction electricity first which means the P wave happens first then the atrium contracts the QRS wave electricity happens first then The ventricle contracts the T wave happens first then The ventricle relaxes who contracts well the atrium can contract and The ventricle can contract but when we say systole in general most of the time we're referring to the ventricle if I want to refer to Atrium I will say atrial systole but if I just say sisterly I mean ventricular same thing with diastole normal blood pressure 120 over 80. where is that pressure it's in the big arteries this is not the pressure in your heart chambers what's the pressure in my heart chambers then let me start with the first number which is systolic in your left ventricle well where do you think you got the 120 systolic from you got it from your left ventricle so it's 120 during cystory how about my left atrium 10 during systole how about my right atrium 5 5 right ventricle 25 mnemonic just remember Uncle Sam and his coins 5 cents then 10 cents and then 25 cents and then I gave you a dollar Nickel Dime quarter dollar these numbers that I just gave you are the systolic numbers if you want the diastolic all of them are almost zero you can say three four five millimeters of mercury no one cares but be careful of the right atrium because since it has to suck in blood through Venus return sometimes it becomes negative which helps suck blood from your ankles up to your heart through Venus return where did it get the negative from don't forget that you're intra-thoracic or intrapleural pressure is already negative so the next organ which is the lung has negative pressure so this organ will acquire similar pressure moreover if you expand your volume will go up but your pressure will go down according to Boyle's Law provided that the temperature is the same and as you know the body temperature stays the same around 37 degrees Celsius so what's the normal blood pressure in big arteries 120 during system the eight during diastole what's the pressure in my left ventricle 120 same during systole almost zero during diastole so if I ask the aorta hey aorta where did you get the 120 from I got from the left vent which makes sense because the left ventricle contracts and pushes the blood here but hey Iota where did you get the 80 from please don't tell me that you got from the left ventricle because the left vertical doesn't have an 80 to give it has zero during diastole now that's something unique to me I am capable of recoiling around that blood as I recoil what's going to happen to the volume decreases what's going to happen to the pressure increases instead of zero during diastere it increases to 80 because of the elastic recoil something that's unique to arteries not to ventricles and this is the cause of the dichrotic notch or the dichrotic inches Ura of the aorta that you see cardiac cycle grafts next what do you think happens to the left ventricular volume as it pushes blood out of it of course the volume goes down but when it's receiving blood into it the volume goes up and therefore we can put everything that we know so far on one graph this is the pressure graph the pressure of The ventricle goes to 120 upstairs and almost zero downstairs systole versus diastere but if you're talking about big arteries like the aorta radial artery brachial artery Etc they go to 120 during systole and 80 instead of zero during the last three thanks to their elastic recoil remember arteries are more elastic veins are more compliant relatively speaking and here is the volume decreasing during systole increasing during diastole it's the volume of the event S1 closure of the mitral antiochuspid valve helps when do they close just before systole just before blood leaves The ventricle and goes to the outside these two valves close to prevent the back flow of blood from The ventricle to The Atrium how about S2 closure of the aortic and pulmonic valves when does that happen just before diasturi just before my ventricle fills with blood to prevent the backflow of blood back to the Venture and here's the EKG remember electrical changes first then muscle contraction electrical changes first then The ventricle contract S1 is here S2 is here where should I put the pathological S3 and S4 well S3 is caused by the gush of fluid volume overload Blood starts to gush here in diastrally because the ventricle is receiving a gush of blood so S3 is here how about S4 just before the following S1 hard sound he recently The ventricle is Contracting and here's history The ventricle is relaxing and receiving blood in contraction in the beginning The ventricle is Contracting but the aortic valve is not opening yet which means The ventricle acts as a closed chamber closed on this side because the mitral valve is closed and closed on the side because the aortic valve is closed and has not opened yet so it's called isovolumetric the volume of the ventricle is the same it could not shorten and shrink after this the Saving Grace the aortic valve will open pew all of that blood will leave The ventricle and go to the aorta rapid ejection everything that goes up must eventually come down reduce each action I'm still ejecting blood at a lower rate conversely in diastere in the beginning everything is closed the heart acts as a closed chamber so its eyes of volumetric relaxation after this the mitral antrikospid valves will open so the blood will gush from Atria to ventricles rapid fit filling followed by slow or reduced filling this leaves a few drops of blood in the Atria so the Atria will contract pure atrial systole to push those few Bloods down to The ventricle now onto the pressure volume Loop why do you call it pressure volume Loop because pressure is here volume is here it's easier to look at the volume first as the volume increases from here to here do you think this is history or diastere if the volume of the ventricle increases of course this is diastere conversely if the volume is decreasing from this point to this point what do you think is happening it means that the blood is leaving the heart leaving less volume inside the heart so I'm decreasing diastere is here systole is here how do you get the blood to be ejected I have to contract first to push that blood in the beginning the heart was a closed chamber ISO volumetric contraction after this the aortic valve open in Pew I ejected that blood rapid filling reduced feeling how do you get the blood to come to you I have to relax first in the beginning it was isovolumetric what do you mean by ISO volumetric I mean the volume did not change from this point to this point I'm still on the same point on the x-axis isovolumetric relaxation after this the mitral and tricuspid valves will open and the blood will gush Into The ventricle and the volume will rise oh by the way the same graph can be used for the right ventricle pressure versus volume how do I know that this is talking about the right ventricle look at this number it's 30. oh it's not 120 yeah this belongs to the right venture or you can do the same thing for the left vendor how do I know it's the left ventricle it's 120 millimeters of mercury that's the stronger thicker ventricle or you can plot the left ventricle against the right ventricle I think you can see the difference between the 120 and the 25. this is the pressure during systole in the left ventricle and this is the pressure during systole in the right ventricle during diastere however both of them are almost zero unlike the big arteries that are capable of elastic recoil let's take it to the next level we agreed that diastere is here because the volume goes up and that system is here because volume goes down before we can get history to happen the heart acted like a closed chamber isovolumetric ventricular contraction before The ventricle was able to receive their blood during diastere it acted as a closed chamber isovolumetric relaxation when did the Saving Grace happened when the aortic valve opened allowing the blood to be ejected and the volume to decrease and then what after the blood gets ejected rapid ejection and a slow ejection theortic valve will close to prevent the backflow of blood to the left ventricle and when the aortic valve closes it gives you a sound it's S2 sound after this The ventricle will start to relax but still the mitral valve is closed so The ventricle acts as a closed chamber eyes of volumetric relaxation until the mitral valve opens and blood flows from left atrium to left ventricle blood is Flowing right here and I'm filling after this the mitral valve will close so that when The ventricle contracts blood does not flow back from the left ventricle to the left atrium and when a valve closes it gives you a sound mitral valve closure gives us S1 what's the highest volume ever in your left vendor It's The End diastolic volume and what's the lowest volume It's The End systolic volume and what's the difference between them it's called the stroke volume example if my end systolic volume is 120 ml and the end systolic volume is 40 ml can you calculate the stroke volume please it's 80 ml 120 minus 40 equals 80. so the distance between this point and this point is literally the stroke volume 120 over 80 is the pressure not in The ventricle but in big arteries this is called systolic blood pressure and this is called diastolic blood pressure the 120 is the same endpoint as the greatest pressure ever in the left ventricle it's called the maximal afterload pressure or the systolic pressure in the left ventric how about the diastolic pressure in the left ventricle almost zero you can call it the left ventricular and diastolic pressure while the left ventricular and systolic pressure is here not quite 120 why not 120 was the maximal point in the midst of systole but if you want the end of systolic pressure it's going to be a little less usually between 120 and 80. if you are a meth not you remember that under every curve there is something called area under the curve that can be calculated through calculus since this is not a curve this is a loop we have area inside the loop it's called The Stroke work I.E the energy required to eject blood in a stroke hence stroke volume hence stroke pressure time from this graph can you calculate the stroke volume the ejection fraction and the systolic blood pressure I mean in a big artery and can you tell me which of these points a b c d e f g Etc represents S3 heart sound and S4 please pause let's answer these together stroke volume is what end diastolic volume minus end systolic volume here is the end diastolic here's the end systolic so it's 120 minus 35 equals 85 85 watt milliliters next ejection fraction each action fraction is what stroke volume I just got that over end diastolic volume my stroke volume is 85 my end diastolic volume is 120 which gives me something akin to 71 percent that is some robust ejection fraction I can tell you that systolic that pressure I.E blood pressure in big arteries during cystory the highest number of cores which is 120 millimeters of murky the point at which S3 is heard S3 is abnormal it's caused by gush of fluid the fluid is gushing the most at E look at this it's called rapid filling baby so it's e how about S4 S4 happens just before S1 and where is S1 S1 is B the point just before it is f as in F me quiz time you have three graphs here which one represents a healthy heart receiving digoxin medication please pause let's try to answer this together let me tell you something you know what's the slope of this graph is you find yourself the point of origin which is the zero point here and you go up up up up until you intersect with this point right here now we have a straight line that you can calculate its slope if you remember from basic math slope equals what rise over run it also equals 10 of this angle which is the angle between that line and the x-axis not the Y not this angle nope nope no problem you'll mess it up this angle right here okay so that's the slope then it's how big the angle is perfect let's compare among these three here is the slope for graph B it's a smaller angle and here is the slope for graph C even smaller angle the slope represents contractility the force of contraction digoxin increases the force of contractility which means you should choose the graph with the highest slope highest force of contraction which is a so let's dot the eyes and cross the t's S3 is here S4 is here S1 is here S2 is here what's the slope of this line it represents contractility if you go this way the angle gets bigger and contractility increases if the entire graph is shifted to the right then the angle decreases and contractility goes down this was the best explanation of pressure volume Loops ever systole diastole S1 S2 pause and review if you want to be an excellent student bring a piece of paper and draw everything on the pressure volume loop from scratch and explain it to yourself as you go do it three times today three times tomorrow and three times next week and you will remember this for a long time this graph is important in physiology it's important in Pharmacology of great importance in Internal Medicine and surgery don't forget to say thank you to Jordan in the comment section if you want to learn more about many arrhythmias heart attacks and strokes download my emergency medicine high yields course at medicosisperfixnetis.com if you want to learn about the normal changes during pregnancy and the abnormal diseases that happen during pregnancy such as gestational diabetes preeclampsia eclampsia acute fatty liver of pregnancy peripartum cardiomyopathy and much more download my OB GYN high yield scores and if you want to learn about antiarrhythmics anti-angino antihypertensive medications and even antihyperlipidemics download myocardiac pharmacology course if you do not wish to download my courses and you would rather watch them on YouTube you can do so by clicking on the join button and choosing the highest tier it will open up more than 300 premium videos for you that you can watch right now at Double the playback speed if you want education is fun please subscribe hit the Bell click on the join button you can support me here or here go to my website download my courses notes and cases be safe stay happy study hard this is medicosa's perfectionist where medicine makes perfect sense thank you Jordan