hi everybody dr mike here did you know your heart beats around about five thousand times in an hour which means it beats around about three and a half billion times in your lifetime now in order for a heart to beat it must contract and in order for a heart to contract it needs electrical stimulus telling it to contract so this video is talking about that electrical stimulus what we term the neural conduction of the heart now what i've drawn up here is a heart and you can see the four chambers of the heart the two atria at the top and the two ventricles down the bottom we've got right atrium left atrium right ventricle left ventricle and the rest all this tissue here is heart muscle and we term that myocardium that's what contracts when it contracts it squeezes blood through these particular chambers into the various veins or arteries all right now when a heart contracts did you know that your heart can spontaneously contract it i could take a heart out of your chest and it could beat by itself now the reason why your heart can beat by itself is because of a specialized set of myocardia right here heart muscle right there and what this specialized group of neuron myocardium like tissue does is it spontaneously fires off it spontaneously sends a signal in actual fact every 60 well around about 60 to 100 times per minute it will send an electrical signal and it begins here at the atrium now because it sets the rhythm of the heart that's what we term the sinus rhythm and because this group of specialized cells sit at the atria it is termed the cyano atrial node also just term the sa node so the sa node starts the rhythm of the heart that we term the sinus rhythm it does it around about 60 to 100 times a minute and it can do it by itself now the brain can impact how fast or slow this beats through a specialized part of the nervous system called the autonomic nervous system that's the sympathetic or parasympathetic fight or flight rest and digest but we're talking about just the sinus rhythm now when it sends that electrical signal actually sends it through the myocardium of the atria and it does it in that fashion sends it out through the myocardium now another important point is when electrical signal is sent through muscle in order for that muscle to contract calcium must jump into the cells so the order is electrical signal calcium jumping in muscle contracts so that sent the signal calcium is going to jump in those atria contract pushes blood down into the ventricles that's initiated by the cyanoatrial node now the next thing is we've got this bit of tissue right here this tissue stops the electrical signal it stops the electrical signal and funnels it to one particular point right here another node another group of specialized cells which sit between the atria and the ventricles and therefore it's called the atrioventricular node atrio ventricular node also just termed the av node now this is important the electrical signal gets stopped at this bit of tissue right here okay and it stops for around about point four of a second so we've got the boom is going to be the next part so this is that pause between the two beats of your heart so it all funnels into the av node and the av node sends the electrical signal down this bundle of neurons that we call the bundle of his bundle of his now the bundle of his branches off into left and right bundle branches left and right bundle branches and these left and right bundle branches go down this septum between the two ventricles that we call the interventricular septum now as it moves down it goes down to the apex of the heart and then up and then you've got various branches going down like this okay these are called purkinje fibers again purkinje because it's named after some old dead white guy but these are the purkinje fibers and they send the rest of the electrical activity into the myocardium of the ventricles and again calcium jumps in and they contract pushing blood out of the heart if it's the right side it goes to the lungs if it's the left it goes to the body so what do we have what's the order of electrical conduction of the heart sa node fires off around about 60 to 100 times a minute it shoots through the myocardium of the atria it gets stopped by this bit of tissue and funnels through the av node that's a break of around about 0.4 of a second the av node if the sa node wasn't there the av node is also a set of pacemaker cells and that fires off around about 40 to 60 times a minute so a little bit less than the sa node then it funnels it down the bundle of his then the left and right bundle branches and then through the piking fibers that send that signal to the myocardium of the ventricles so kelsey can jump in and those ventricles contract so this is the neural conduction of the heart hi everybody dr mike here in this video we're going to take a look at how the sa node which is the sinoatrial node and the av node which is the atrioventricular node how they send their signal their electrical signal that we term an action potential to the rest of the muscle of the heart to tell it to contract so what we need to go through is firstly if i were to draw the heart up itself and just very quickly i've got the heart here we know that there's a fibrous bit of tissue here that separates the atria the two chambers at the top and the ventricles the two chambers at the bottom and we know that there is a specialized type of myocardium which is heart muscle cell a very specialized type that sits at the back of the right atrium that we term the sa node now these cells spontaneously depolarize what's that mean it means they spontaneously send an electrical signal they actually do this around about 70 to 100 times a minute and when they send this signal they spread the electrical signal to the surrounding heart muscle tissue in a fashion like that now as it spreads that signal through what we term the myocardium the heart muscle of the atria that then tells the heart muscle to contract and they squeeze and push the blood down into the ventricles now the electrical signal wants to spread down into the ventricles but it can't because of this fibrous bit of tissue here but the electrical signal can bottleneck itself through another specialized group of myocardium that we now term the av node the atrioventricular node and the action potentials are being pushed through this av node and therefore the heart muscle doesn't contract for 0.1 of a second there's a break between the atrial contraction and the ventricular contraction of 0.1 of a second this gives the heart enough time for the ventricles to fill with blood after the atria contract once that point one of a second has occurred and the action potential spreads down the av node it goes down into what we call the bundle of his and that spreads to two the left and right bundle branches and then they send electrical signals through the ventricular heart muscle and as it spreads through that action potential then tells the muscle to contract and blood gets squirted out if it's the right ventricle it goes to the lungs if it's the left ventricle it goes to the body so what we're talking about is today the av node sorry the sa node and the av node how do they send their electrical signals if i said the av nodes spontaneously depolarized they just basically stimulate this action potential all by itself how does it do it well let's first have a look here actually let's have a look here at a cell of the sa node so i said they're specialized myocardium so it looks a little bit different here compared to normal myocardium but it's connected you can see there's a conversation that can be had between the sa node and the myocardium now the first thing you need to be aware of is that all cells of the body have a very special pump called the sodium potassium atpase pump let's draw this sodium potassium atpase pump right here and what it does is it uses atp we know atp is the energy currency of the body uses atp to throw three sodium out of the cell and throw two potassium into the cell now i want you to think about that if we throw three positive sodium out of the cell and throw two potassium into the cell where do we have a net positive charge well we've got three positive things outside two positive things inside the net positive charge is outside which means the net negative charge is inside and if you were to compare those charge differences what you'd find is inside compared to outsize outside is negative five millivolts okay so on this table here where we've got zero millivolts down to negative ninety millivolts up to positive twenty negative five millivolts is only around about here now this isn't all that's happening but what is happening due to this is we're accumulating a whole bunch of sodium outside the cell and we're accumulating a whole bunch of potassium in the cell that's the first thing second thing is this this cell is quite leaky to sodium sorry to potassium and if it's leaky to potassium we're going to have potassium leak out of the cell very slowly now if positive potassium is leaking out of the cell it becomes even more negative inside right because positive things are going out so it goes from negative 5 actually all the way down to around about negative 55 and so we've now got around about negative 55 a charge difference inside compared to outside so inside negative 55 compared to the positive outside now another thing that's happening is this these sa node cells are leaking not just to sodium potassium but they also leak it to sodium and calcium so what you'll find is this you can have some cells here let's draw this as a square you're going to have some channels here sorry that are leaky to calcium and i want you to think about this calcium sits predominantly outside the cell and it will leak into the cell which brings a positive charge inside in actual fact there's also leaky sodium channels which bring positive sodium into the cell as well now you're probably getting confused here we've thrown three sodium out two potassium in but potassium is leaking out making it negative inside but we've also got calcium and sodium leaking inside making it positive inside it doesn't know what charge it is in actual fact what that means is this it starts its baseline is around about negative 55 but because of the leaky calcium and sodium it actually is always drifting drifting drifting drifting up towards the positive because all this calcium and sodium is slowly drifting in now in actual fact there is a mark right here at around about negative 40. now this mark at negative 40 is what we term the threshold and it's the threshold for what another group of channels what are these channels they're another type of calcium channel at negative 40 this is the key that unlocks this new type of calcium channel a faster calcium channel and when that opens up more calcium rushes in and when more calcium rushes in what we get is a fast stimulus up to around about positive 20. now when it hits as this is happening going up to positive 20 what you'll find is that at around about positive 20 more potassium channels open up remember these were just leaky potassium channels now we've got very specific potassium channels opening up and heaps of potassium start to leak out of the cell now if heaps of potassium leak out of the cell at positive 20 the positive is going back out again and it drops back down to around about negative 55 to negative 60. now if it's dropping back down to here what happens again the whole thing occurs leaky calcium leaky sodium and then it goes back up to negative 40 which then opens the calcium channels and that sends the signal back up which closes the channels but opens the potassium channels and it drops back down so what do we have here basically to summarize we've got at this point here it's sodium and calcium leaking in at this point [Applause] we've got calcium shooting in and at this point we've got potassium going out now what we term this is this part is depolarization this part is repolarization depolarization repolarization and this is what's happening at both the sa and av node and as you can see it just spontaneously does this and it does it at the sa node it does it around about 60 to 100 times per minute and at the av node it does it around about 40 to 60 times per minute and this is what we term the pacemaker cells of the heart so these are the action potentials of the sa node and av node hi everyone dr mike here in this video we're going to talk about how the nervous system can control the heart rate and contraction so first thing we need to talk about is we know the sympathetic and parasympathetic divisions of the autonomic that's automatic nervous system you don't control this consciously but the sympathetic nervous system is that fight or flight it gets stimulated in times of stress or fear and the parasympathetic nervous system is the rest and digest that gets stimulated in times of digesting and relaxation because we know exactly what happens to our body in these scenarios you should know which one causes an increase in heart rate and contractility and which one causes a decrease in heart rate well sympathetic fight or flight what happens when you're scared heart rate increases and the contractility or the force of the heart rate increases as well now this is sympathetic innovation let's take a look sympathetic innovation is going to begin for the heart at the cardio acceleratory center it's a big name but this is the part that controls the speed of the heart it is here at the medulla so remember your brain stem right your brain stem has the midbrain pons medulla and this is the cerebrum the chunk of the brain so midbrain pons medulla lowest part of the brain stem is the medulla and at the medulla you've got a specific area dedicated to increasing the speed of the heart called the cardio excellatory center and we've got sympathetic nerve fibers present as you can see here what they do is they send a signal down the spinal cord until it hits the thoracic one two three and four area so your thoracic one two three four as you can see here and shoots a signal out to what we term the paravertebral ganglia okay so for the sympathetic nervous system there is a group of cell bodies that sits outside the spinal cord that we term the para meaning next to vertebral so next to the vertebrae ganglia just meaning a group of cell bodies outside the central nervous system and this is where the sympathetic nervous system synapses with their neurons okay with the next neuron and you can see that happening here first neuron shoots out t1 to t4 and then synapses with various cell bodies of the next sympathetic neuron here at the chain at the paravertebral ganglia now they send this now they go up and down right and they send their signals out going towards the heart like i said this is a sympathetic nerve fiber or nerve fibers go into the heart and where does it innovate it innervates the sa node it innervates the av node and it innervates the myocardium of the ventricles so i'll say it again the sa node sets the rhythm of the heart it spontaneously sends signals between 70 to 100 times a minute this is what sets the pace or rhythm of your heart the av node if the sa node cramps itself the av node will kick in and that spontaneously depolarizes around about 40 to 60 times a minute so a little bit slower so that's the reason why the sa node sets the rhythm because it just does it faster than the av node okay now the muscle if you've got sympathetic nerves innervating the muscle it's going to tell them to contract harder so sa node and av node speed musculature contractile force so the sympathetic nervous system when it sends a signal down it's going to release noradrenaline or norepinephrine if you're in the states and this noradrenaline what it's going to do is this the noradrenaline will so this is the cell of these nodal cells right sa node or av node and you know already that there's heaps of sodium outside the cell there's heaps of calcium outside the cell and there's heaps of potassium inside the cell and if i were to measure the charge difference between outside and inside we know inside is more negatively charged compared to outside if you're unsure why watch one of my previous videos inside is actually sitting at around about negative 55 millivolts compared to outside and we know if we want these sa or av nodes to send signals through the heart they need to hit negative 40 that's the threshold now to go from negative 55 to negative 40 that's going more positive negative 55 is more negative than negative 40 right so to go from negative 55 to negative 40 positive things need to go into the cell what are the positive things sodium and calcium now if enough sodium and calcium go in it hits negative 40 we've hit the threshold that opens up a whole bunch of more calcium channels and huge amounts of calcium shooting making it really positive inside the cell and now what we've done is we've sent an electrical signal through the sa node and the atria now what does sympathetic neurons do the sympathetic innovation when it releases adrenaline or noradrenaline it binds the specific receptors here that are called beta-1 receptors beta-1 receptors are located at the sa node av node and the myocardium and what they do is they let sodium and calcium in allowing for this to happen more frequently hence the heart rate increases that's the sympathetic neuron what about here at the myocardium is it doing the same thing well myocardium in order for it to contract it only cares about calcium so what happens here is it more specifically allows for more calcium in calcium into the cell increased contractile force so that's how the sympathetic neurons tell the heart to increase its contractile for so sympathetic increase heart rate increase contractility beautiful now what about the parasympathetic rest and digest it slows the heart down now this is coming from again the medulla but the dorsal aspect of the medulla and this is the cardio inhibitory center and when the sympathetic neurons get activated they can synapse with an interneuron that's simply a neuron that's the intermediate between one and another and that synapses with neurons of the parasympathetic nervous system or more specifically the vagus in the dorsal or back aspect of the medulla this then fires vagal nerves out now the vagus nerve is a cranial nerve so it doesn't go down the spinal cord the vagus nerve comes out of the head and neck okay and as you can see it's shooting out and what it does is it innervates the sa node and av node and rarely or not many fibers innervate the musculature so i haven't drawn it in so the main effect of the inhibitory signals from the parasympathetic neuron specifically the branches of the vagus is that it goes to the sa node and av node and tells them to slow their signals down when you think about this how does or how could it tell this must this nodal cell to slow its firing down i told you to increase it more positive things need to go in so what do you think to decrease it again remember in order for it to send a signal it needs to hit negative 40. so it needs to become positive inside but to slow it down to make it harder to send a signal what you could do is send positive things out right and what do we have inside potassium so what the parasympathetic fibers do more specifically the vagus when it innervates the sa node and av node it releases acetylcholine so i said sympathetic release noradrenaline the parasympathetic released acetylcholine and that told potassium to leave the cell this positive stuff is exiting which means it goes from negative 55 even lower now when it goes even lower the distance that it needs to then go from let's just say negative 60 or negative 65 to negative 40 is far greater than negative 55 to negative 40 which means you need way more positive things coming in it makes it harder to send a signal harder for the heart to contract harder for the heart rate to increase so the way the parasympathetic nerve fibers do it they release acetylcholine to the sa and av node it increases the efflux of potassium out of the cell making it more polarized that's called hyperpolarization which means it makes it more difficult to depolarize and therefore slows the heart down so this is how the central nervous system tells the heart to speed up or slow down so in this video we're going to have a look at ecg placement now firstly what does ecg stand for it stands for electrocardiogram or electrocardiograph and it's a way of measuring the electrical activity of the heart remember that the heart's a pump it's a muscular pump that when it contracts it will push blood either from the atria to the ventricles or from the ventricles out of the respective arteries now before it can contract electrical signals need to be sent down through this muscle tissue and ecg's measure the direction that these waves move okay now what we're going to look at today or very quickly in this video is what we call a 12 lead ecg okay now please be aware that leads are different to electrodes the electrodes are the sticky dots that you place on the patient the leads are basically the set of eyes on the heart having a look at what's going on giving you the ecg readout okay so in a 12 lead ecg we have 12 views of the heart but in actual fact we only only use 10 electrodes to get these 12 views okay so what i'm going to do now is just show you exactly where these 10 electrodes go and then in the next video i'm going to have a look at how these electrodes view the heart differently so of the ten electrodes you are going to find that four of them go in your limbs one on the left hand one on the right hand one left leg one left leg a right leg there are four electrodes the other six of the ten electrodes go on the chest and they're called the precordial electrodes and they also the electrodes that give you the precordial leads or precordial readouts so first thing i want to do is draw up the chest so what we're going to do is first of all draw the sternum just very simply and draw the sternum we're going to draw the clavicle we're going to draw some ribs maybe six or so ribs one two three four five six okay now when we place these what we call precordial electrons we have six we start with the first one and we call the first one v one now where does v1 go remember please remember that when you're looking at the patient that's the right side that's the left hand side and you know that the heart sits upon the sternum a little bit to the left turned a little bit so the apex or the point of the heart is pointing towards the left hip so you need to keep that in mind because that's important when it comes to the placement of these leads of these electrodes okay v1 first electrode we place from the sternum go to the right of that sternum and then count your ribs go to your fourth rib and after that fourth rib is your fourth intercostal space so that's one two three four so to the right of your sternum at the fourth intercostal space one two three four we place the first electrode v1 now v2 is very easy because it goes again at the fourth intercostal space but on the left hand side of the sternum so that's where v2 sits now usually you'll skip v3 and i'll show you why in a second and move to v4 to find where v4 goes you find the clavicle and go mid clavicular and you'll move down to the fifth intercostal space okay and that fifth intercostal space if you feel you should be able to feel your heartbeat what you're actually feeling is the apex of your heart hitting the precardium okay that's the fifth intercostal space and that's where you put v4 so mid-clavicular fifth intercostal space v4 v3 simply goes immediately between v2 and v4 and v5 and v6 very easily go at the fifth intercostal space but move towards the axillary the axillary is the underarm okay so that means we will also put v5 and v6 okay they are the precordial electrodes giving you the precordial leads the electrodes you place on the chest of your patient now what about the other four because i said there's ten electrodes well if we were to draw up just the stick figure of an individual you will place one lead or one electrode i should say left arm right arm left leg and right leg now you can see i drew three the same color and one a different color now the three of the same color right arm left arm left leg that's important because what you can see is the right leg which i drew in red actually does not contribute to the ecg in regards to its view of the heart it's not a lead does not give us a view of the heart it is a ground for the machine okay sort of gets rid of some of that background so what you can see is one two three electrodes right arm left arm left leg they contribute to the views of the heart okay now this is where they're placed now you need to remember that placing them here so if i were to draw the trunk of this individual okay so i'm drawing the trunk of the individual that placing a lead on a patient's arm is basically the same as placing it at the trunk where that limb connects okay so whether it's here or here or here now the reason why this is important is because remember we have the heart placed in here roughly and what we have is the left arm lead is going to have its own little view of the heart the right arm lead is going to have its own little view of the heart the left leg leads going to have its own little view of the heart but in addition to that what you'll find is that unlike the electrodes on the chest these electrodes can speak to each other okay they're called bipolar leads these are called unipolar leads now that means that the right arm can speak to the left arm the right arm can speak to the left leg or left foot and the left arm can speak to the left foot okay so right arm speaks to left arm right arm speaks to left leg and left arm speaks to left leg the reason why this is important is because when they talk to each other they also measure what's going on in regards to the electrical activity of the heart in that particular direction okay so in addition to having a view of the heart view of the heart view of the heart from these electrodes we also have a view of the heart basically from this direction because of this one coming across we call that limb lead one where we view the heart from this direction we call that limb lead 2 and we have one from this direction so this one going across like this we call that limb lead 3 we don't call this lead because it's a view of the heart it's a lead now not an electrode we don't call this lead right arm we call it a v r which stands for augmented vector right arm don't stress out about that too much we don't call this one left arm we call it augmented vector left arm and we don't call this left leg we call it a v f which is augmented vector foot so that looks a little bit messy if i were to just draw this up just here just a little bit larger it means that we now have a view of the heart if i get rid of this very quickly we have a view of the heart from there from there from there so it's going to be avl avr this is going to be avf we also have a view of the heart from here which is lim lead one a view of the heart from here which is lingling too and the view of the heart from here which is lim lead three how many views of the heart is that that's one two three four five six views of the heart from four electrodes so four electrodes on the limbs give you six views of the heart plus the six views of the heart you get from the pre-chord you'll give you 12 leads that's your 12-lead ecg please remember these legs on the chest they're placed on the chest like this so they're viewing the heart from that direction these limb leads are viewing the heart from this direction so what do we have we've got a view of the heart from here and a view of the heart from here we now have a 3d view of what's going on electrically in the heart okay in the next video i'm going to talk about this in a little bit more detail so in this video we're going to have a look at an ecg readout and what that readout means physiologically when we look at the heart so let's say you've got your patient patients lying down you have the ecg machine let's say you have a 12 lead ecg which means you have the 10 electrodes placed on your patient if you're unsure where these 10 electrodes go please watch the ecg placement video so you've got these 10 electrodes placed on the patient which is giving you 12 views of the heart and again these give you 12 individual views as to what's happening in regards to depolarization and repolarization events and again i've done another video looking at depolarization repolarization okay first things this we're just going to take one example lead so let's say we have a lead that's placed here so it's looking at the half in that direction right so you can pretend that it's looking up at the heart and this set of eyes here let's say it's lead v5 or lead 2 will give you a view of the heart from around about this angle okay let's look in the heart from this angle like this okay so that means whatever is happening in its direction or whatever is happening away from it electrically it's going to see and it spits out some sort of reading so let's have a quick talk about that generally what you're going to find is that the heart in a healthy individual we'll begin its contraction starting at this little group of specialized myocardium a group of specialized heart muscle cells in a little area here which we call the sinoatrial node the sa node okay now these group of cells automatically or spontaneously depolarize okay what does that mean i showed you in the heart muscle cell depolarization repolarization video that when you have a cell that you have sodium channels and sodium ones that come in and you have potassium channels and potassium wants to come out that's so potassium wants to come out i told you that some stimulus needs to happen in order to open the sodium channels to let it in well with these cytolateral node nodal cells there doesn't need to be an external stimulus they have already some sodium channels open which means sodium trickles in at all times now remember what that means i told you so you have to remember with that graph when the cell's at rest that's negative 90 you have a threshold of negative 70 and you have a maximum around about positive 20 positive 30. go back to the video looking at heart muscle repolarization depolarization cells at rest nothing's happening some sodium channels open up and some sodium starts to come in and it shifts up into the positive until it hits negative 70. then it depolarizes i told you for every other heart muscle cell it needs a stimulus in order for that portion to happen except the cells of the sinuage you'll know they always they spontaneously hit depolarization they spontaneously hit the threshold okay so we have these cells these cells of the sinoatrial node and they've started to depolarize now remember what that means the polarization is sodium coming in sodium's positive so you get a wave of depolarization which is a wave of sodium coming into the cell and i told you one heart muscle cell's connected to another connected to another connected to another which means when sodium comes into one cell it trickles through sodium comes into next trickles through it comes into next that's why it's a wave of depolarization when these cyano the cells of the cyanide and i depolarize they depolarize i get across all the myocardium of the atrium in this direction okay that's the wave of depolarization meaning all those cells are connected to each other sodium comes in goes in that direction which means remember it's going from inside the cell negative to positive which means you have a wave of positive stuff going in that direction like that okay so first thing is this you need to have a look at the lead and where the lead is looking at and then have a look at the depolarization event and see where that's going to if you see that the lead is looking at the depolarization event or the depolarization event is happening in the direction of the lead what you will find on your ecg readout is every time depolarization happens in the direction of the lead you will always get a bump up on the lead okay let's have a look at the cheat sheet that i always tell you about okay so if you were to draw one lead two leads three leads four legs draw four leads for me if depolarization occurs in the direction of the lead and depolarization as you can see is positive stuff coming into the cell if this happens in the direction the lead you will get a bump up on your ecg okay so under that logic thinking via that means if depolarization therefore occurred away from the lead what do you think the ecg readout would give you well if positive towards gives you up then positive away should give you a downward deflection okay okay let's make it a little bit more difficult what if so this is depolarization what about repolarization so let's just say this all the muscle of the atria have now depolarized become positive and then contract contracts because i told you that depolarization precedes calcium influx which then leads to contraction and then repolarization occurs meaning the potassium comes out and becomes negative again okay so if we wanted to reset this and repolarize this heart muscle cell that means negative stuff moving around what if repolarization happened in the direction of the lead so again use the same logic you've been using if positive stuff in the direction lead gives a bump up the negative stuff in the direction lead should give you so positive and negative opposite so if positive stuff in the directionally gives you a bump up negative stuff in the direction of the lead should give you a bump down so a deflection in the ecg readout and again using the same logic what if repolarization happened away from the lead repolarization away from the lead well it's going to be the opposite that's the opposite it's going to be a bump up okay this is the cheat sheet for an ecg this tells you what's going on so again let's look at this either v5 or lead ii it's viewing the heart from this direction the sinoatrial node it's stimulated the depolarization event automatically spontaneously it's happened and it sends a wave of this positive depolarization through the heart in that direction like that and this is in the direction of the lead overall you can see that it's going in the direction of the lead and if depolarization goes in the direction lead you get a bump up okay all right next point once that's happened it hits this fibrous tissue there is a fibrous atrial ventricular septum separates the atrium from the ventricles and it stops the depolarization wave so depolarization cannot move through so it stops it so once that's happened no positive stuff's moving through the atria or the ventricles so you get a flat line because there's no positive or negative stuff moving anywhere the lead won't pick anything up so you have a flat line next thing is this there is an actual fact another group of cells similar to the sa node that sit right there now that's the sa node cyanoatrial node sets the sinus rhythm this is the av node the ventricular node because it sits between the atrium and the ventricles okay so this av node once the depolarization wave is spread through the only place that it can continue through from the atria it can't get through this fibrous septum it can only slowly travel through the av node very slowly takes point one of a second so that means that the polarization of the atrium then contraction then there's a 0.1 second break while the depolarization wave moves through and then it continues to propagate you have a flat line while it's propagating through so once that's happened once the action potential or the depolarization event has moved through this av node branches off like this okay and the left branch now this is called the bundle of hiss okay the bundle of hiss branches into the left and right purkinje fibers but the bundle of hiss you'll see the left branch branches off like that okay so that means once this depolarization event has reached the av node flat line it then propagates through these fibers now these fibers are really fast okay very very fast and as the depolarization wave spreads down as it goes down you can see that it goes down like that but also down the left bundle and starts to fire up like that all these branches firing up so it depolarizes the septum between the left and right ventricle like that in that direction you can see in that direction that means positive stuff is moving in that direction so that means look at the lead is this depolarization event going towards the leader away from the lead overall away from the lead because as it moves down these ones are going up like that okay so that means what you get is depolarization away from the lead a deflection a bump down now this deflection isn't nice and rounded like that because these fibers are very fast and because it's not a thick tissue it doesn't last very long you get a bump down like that okay all right once the depolarization event has reached towards the apex these bundle branches move through and turn into picking fibers that move up like that and these purkinje fibers branch off like that okay so that means it's depolarized down we get a deflection because it's going away for the lead then it reaches here and what you'll find is it starts to depolarize like that so have a look is that overall in the direction of the leader away now you may think well this part's in the direction of the lead so the left ventricle is but the right ventricle is going away from the lead so you may go i don't know what direction this is happening well remember the left ventricular wall is about three times thicker than the right so what's happening in the left ventricular wall is going to overpower what you read on the ecg to what's happening on the right so what's happening over here predominantly the depolarization event which is positive stuff is going in the direction of the lead and because the tissue is thick and they're very fast fibers you get a very high bump up like that okay now once it's reached to the what we call towards the base so remember that's the base of the heart that's the apex once this depolarization event has reached towards the base of the ventricles the depolarization event moves up like that so this is the part we're looking at now you can see it moves up and away so we have depolarization going away from the lead it's not a very big bit of tissue and they're fast fibers so we get another deflection another bump down cool all right what's the next part we have now just depolarized the entire heart it's all positive now right and it's all contracted so sodium comes in calcium contracts sodium comes in calcium contract now what do we need to do well we need to repolarize it okay that's where the so that's where the potassium leaves the cell to make it negative again inside okay so that means we need to make all this negative again now what you need to realize is this even though depolarization started here and moved like that and then went to the av node and moved like that and then like that repolarization does not start where depolarization started repolarization starts where depolarization finished up here okay which means now repolarization goes in this direction okay re-polarization goes in this direction so as it goes down you all you need to do is look at the opposite of the d-pole it goes in the opposite direction to depol and you saw d-pole predominantly go in that direction for that big bump so repolarization goes in the opposite direction okay and that's going making it negative again so you can see this is happening away from the lead right so we have a repolarization event going away from the lead what do we get we get a bump up and this is your ecg that's going to reset now that's going to go back to negative and then the next cycle can happen so this is one cardiac cycle this is one boom boom resets boom boom resets boom boom resets boom boom okay so this is what we call just a general ecg readout and you can see it's basically an ecg readout from the v5 or lead 2 cable so what does that mean overall it means this if we look at this first wave this first wave represented atrial depolarization okay the next big complex here represented overall ventricular depolarization okay and then the last bump represented ventricular repolarization and that's what an ecg is measuring now you may ask okay atrial depolar ventricular depolar ventricular repol where's atrial reed pole it actually happened while ventricular depolarization happened because think deep hole depol when that did that that report and because the ventricle walls are so much thicker it basically is hidden the atrial repolarization is hidden behind the ventricular depol now these peaks and troughs have little symbols associated with them okay letters of the alphabet h or d pole the first wave is called the p wave the first little dip here is called the q wave then r then s then t which means atrial depolarization is represented by the p wave ventricular depolarization is represented by the qrs complex and the t wave represents ventricular repolarization and that's all from the view from the v5 or lead 2. think about if the lead is up here so the avr lead what if the avr lead was up here looking at the heart from that direction what do you think would happen it's meant it's just looking at deep hole or repo events either away or towards it views the heart from the opposite direction so what do you think the ecg readout should look like it should look like the opposite the inverse and it does an avr readout should look like this the opposite okay i'm going to do another video just probably condensing all this in a very quick summative form but i hope all this made sense hi everybody dr mike here in this video we're going to take a quick look at cardiac output and all the factors that contribute to cardiac output now what is cardiac output well simply put it is the amount of blood that our heart pumps out every minute now in order to calculate this there's two major factors that are involved well it sort of makes sense to think if we need to calculate how much blood's pumped out per minute that we need to know how many times the heart beats or pumps in that minute and how much blood the heart ejects every beat or every contraction these are the two major factors now first one being the heart rate and our heart rate on average is around about 70 beats per minute and the amount of blood that our heart ejects every beat or every contraction that's termed the stroke volume and that's around about 70 mils again this is on average so if you calculate 70 beats per minute times 70 mils what you get is your cardiac output in a minute and that ends up being around about 5 liters per minute that's our cardiac output now obviously these values are the average and for some individuals like athletes you'll find that their heart rate is significantly lower can be around about 50 beats per minute so in order for them to be able to pump out 5 liters a minute their stroke volume must be higher and it is it can be about 100 mils and what that means is the heart becomes more efficient less beats but with every contraction more blood is ejected out now if we have a look at all the factors that contribute to these two heart rate and stroke volume what you'll find is this heart rate being the speed or how many beats per minute that's influenced by certain hormones in the body and innervation of the body predominantly we're talking about the autonomic nervous system here we're talking about the rest and digest and the fight or flight system also known as the parasympathetic and the sympathetic nervous system they can affect the heart rate but when we look at the stroke volume the amount of blood ejected every beat there are three major factors here one of which is contractility this is the forceful contraction of the heart this is about recruiting muscle fibers and the contraction of that heart another one is something termed pre-load now preload has to do with the stretch of the ventricles of the heart just before it contracts just before it contracts and ejects that blood out i want you to think about it like this when we take the heart if we were to feel the heart so remember this when the hearts relax this is called diastole under diastole the heart's relaxed and it starts to fill up with blood all right now at the end of this relaxation point it's termed end diastolic volume end diastolic volume is the amount of blood that has filled the heart at the end of relaxation all right so basically it's going to be the maximum volume of blood in the heart all right at any one moment esv is end systolic volume systole is the contraction of the heart therefore end systolic means right at the end of the contraction so once the heart is finished contracting the end systolic volume is the amount of blood left over in the heart after the contraction so think about it end diastolic volume it's at the end of relaxation the heart is filled up it's the maximum volume of blood available then the heart contracts when the heart contracts it's going to eject that blood out when it ejects that blood out at the end of that forceful contraction there's going to be some blood left over in the heart if you take the maximum volume of blood in the heart and you deduct the amount of blood left over in the heart you end up getting the value of the stroke volume which is the amount of blood that has been ejected now contractility preload and afterload effect end diastolic volume and end systolic volume and therefore effect the stroke volume now i told you about contractility that's the forceful contraction of the heart the harder you contract the more blood you eject out okay therefore increased stroke volume preload which is what i was getting to preload is referring to that stretch during end diastolic filling so the heart under diastole so it's relaxing is filling up as it fills up it's stretching the walls of the ventricles now at the very end of filling the ventricles are at its maximum stretch this is preload and the reason why this is important is because the more you stretch the walls of the ventricles the more those ventricles will contract back and eject blood out this is called the frank styling mechanism the frank styling mechanism or theory again states that the more you stretch the heart the greater the heart will contract and eject blood out therefore the greater the stretching or greater the feeling the more blood that will be ejected so that's what preload is referring to the stretch on the walls of the ventricles so if you increase preload you will increase the amount of blood eject and therefore increase stroke volume so increase contractility increase stroke volume increase preload increase stroke volume but now we're going to talk about afterload and afterload is different when we take a look at this heart again you've filled the heart up so we've got the end diastolic volume it's filled up and we want to eject that blood let's just say out of the aorta for example we need to contract the walls of the ventricles but there is going to be some resistance experienced in the aorta in the artery that's go that blood is going to move through now this resistance can be great or can be minimal if for example somebody has some plaque built up in the walls of that artery you've narrowed that tube and therefore increase the resistance think about it you put your thumb on the end of a hose you're increasing the resistance it's harder for that fluid to move through same thing's happening here that is afterload afterload is the resistive forces that this blood or the ventricles need to overcome to eject the blood out okay i'll say that again afterload is a resistive force that the ventricular walls need to overcome in their contraction to push that blood out therefore if afterload is higher stroke volume is usually going to be lower if afterload is higher the ventricles need to contract harder if the ventricles contract harder over time the muscular wall of the heart gets thicker and that's called hypertrophy it becomes thicker so it can contract harder to overcome increased afterload alright so again just to quickly run through cardiac output is heart rate multiplied by the stroke volume and stroke volume is influenced by contractility preload and afterload which therefore means there are four factors that influence the amount of blood that a heart pumps out per minute that is heart rate contractility preload and afterload and that is a quick run through of cardiac output hi everyone dr mike here in this video we're going to take a look at preload and see how preload influences cardiac output remember cardiac output is the amount of blood our heart pumps out every minute and it's around about five liters every minute now preload it's one of the factors that influences stroke volume what stroke volume stroke volume is the amount of blood our heart pumps out every contraction so you obviously multiply that by how many times we or our heart beats per minute and we get our cardiac output all right preload what is it well first thing i need to draw up is a heart and when we have our heart we're also going to have some blood vessels but the only one i'm going to draw up here is going to be the aorta now i want you to think about this your heart's going to contract that's called systole when it contracts it ejects blood and then it relaxes and that's called diastole and that's when it fills with blood we're going to talk right now about diastole the heart is relaxed and it begins to fill up with blood what you'll find is right at the very end of diastole okay so it's right at the end of filling immediately before the heart contracts in systole to eject the blood you've got the end diastolic volume that's this right here and that is going to be the maximum filling of the heart but it's also the maximum stretching of the walls of the ventricles of the heart just before contraction this is actually preload preload is the maximum stretch of the walls of the ventricles or the musculature of the ventricles just before they contract to eject the blood you're probably thinking why is this important for us to understand cardiac output and the reason is because the preload or the maximum stretch of the walls of the ventricles is proportional to the amount of blood that gets ejected out of the heart this is called the frank styling mechanism the frank starling mechanism and it basically states the more you stretch or fill the heart with blood the stronger that contraction is going to be and the more blood gets ejected that means the higher the preload so the higher the stretch the greater the stroke volume the greater the stroke volume the greater the cardiac output so preload is directly proportional to cardiac output more feeling more contraction more ejection okay now things that can affect preload include well the major thing that affects preload is venous return so obviously you're going to have your inferior superior vena cava that's returning deoxygenated blood from the body back to the heart and if you have a greater feeling you're going to have a greater preload if you have a greater preload you're also going to have a greater stroke volume and a greater cardiac output but think about this if the heart rate starts to pump faster faster faster faster there's less time for diastere diastole so that's less time for filling which means a reduced preload and also a reduced cardiac output so you may think but wait a minute an increased heart rate should increase cardiac output and that's true but if the heart rate increases too quickly there's less time for filling and a smaller ejection fraction so a smaller stroke volume so it is complex but all you need to be aware of is for preload it is the maximum stretch on the walls of the ventricles immediately before contraction the greater the stretch the greater the ejection the greater the ejection the greater the cardiac output that's preload hi everybody dr mike here in this video we're going to take a look at afterload and the effect that afterload has on cardiac output now we've spoken about all the other factors involved in cardiac output we've said that cardiac output is the amount of blood our heart pumps out per minute and it's determined by how fast our heart beats and how much blood our heart ejects per beat now we spoke about preload in a previous video that's the maximum stretch on the walls of the ventricles immediately before it contracts to eject the blood out afterload is the amount of resistance or force that these ventricular walls need to overcome in order to eject that blood out of the heart i'll say that again preload is the maximum filling of the heart at the end of diastole it's the maximum filling immediately before contraction pumping that blood out afterload is the force or resistance that these ventricles or muscular walls of the heart need to overcome in their contraction to eject the blood out of the heart now you need to think about what could potentially be resistive forces well think about the aorta for example the aorta is the major artery exiting the heart to deliver blood to the body there's going to be resistance in this vessel why well because there are certain diameters certain perimeters certain boundaries of this aorta that limit the flow coming out and what you'll find is that some individuals as they get older they can have a buildup of plaque or a stenosis or a hardening of the walls of this artery and it narrows the lumen or the hollow inside which means you increase the resistance just like putting your thumb on the end of a hose you're increasing the resistance and it's harder for the fluid to leave that means that the muscular wall of the heart needs to contract harder in order to overcome that resistance okay again afterload is the amount of resistance or force that these ventricular walls need to overcome to pump that blood out if the resistance is higher so that means if afterload is higher it means the ventricular walls need to contract harder to overcome it now the heart's a muscle when you're in the gym and you start to lift heavier and heavier weights those muscles have a greater force or resistance they need to overcome and what do they do they grow larger the heart's exactly the same the heart needs to grow larger or thicker gets a thicker muscular wall simply so it can contract harder to overcome the resistive forces in those tubes that the blood needs to exit okay now this can be a problem because the greater or thicker that wall becomes over time the more blood or oxygen needs to be delivered to that wall in order to maintain it to be healthy but if that continues over time to be an increased resistance or increased afterload so if afterload remains high over time this wall gets thicker and thicker and thicker in order to overcome it which means its own oxygen demand becomes higher and it hits a point where it can't supply its own oxygen demand and the heart muscle begins to die or it doesn't work as a pump and that's heart failure okay so afterload is important for cardiac output because it's the amount of force that these ventricular walls need to overcome to eject that blood out if the aorta is narrowed for whatever particular reason it's harder to eject the blood out so the muscular wall gets thicker if this is maintained over time it becomes more or it has an increased demand for oxygen and it hits a point where it cannot supply its own demand and the individual can go into heart failure so afterload is an important concept to understand when we look at cardiac output there are some drugs that help with this drugs such as beta blockers beta blockers help to relax the heart and therefore reduces the workload of that heart maybe calcium channel blockers as well because remember the more calcium in the muscle cell the stronger the contraction so just be mindful of the importance of afterload in cardiac output