Cardiac Cycle and Conduction Pathway

all right we're going to have a short lecture here just to talk about the cardiac cycle and the conduction pathway how does the signal travel through the heart and then what are the methods and the techniques that we use to be able to look at that and determine what's going on with the heart both at a resting state and during a state of stress something like exercise this is really important for when we're talking about the clinical population and understanding how the heart functions so the heart contraction by way of something known as autoc conduction so autoc conduction means that it has its own built-in electrical pathway that allows it to conduct this electrical impulse all the way from the top of the heart down to the apex of the heart so that we can get the heart to contract and work as one unit so there's no external signal or stimulus that's required and it starts all the way up in your atriums and sends a signal all the way down through the Atri through the ventricles and it comes back up through the ventricular walls and we start the contraction that squeezes the blood back up and out of the heart now as long as your auto conduction is working appropriately then we end up seeing that our intrinsic rate of our contraction is around 60 to 100 beats per minute remember we'd like to see that somewhere between 60 and 80 but the acceptable range is 60 to 100 now when we look at the cardiac induction system let's flip to this slide right here the signal starts up here in something known as the sa note so it's your sinoatrial node and the SA node is also known as the pacemaker of the heart and what that means is it's the one that's initiating the signal so it starts a signal and it sends it down here to something known as the atrioventricular node or the AV node and the job of the AV Noe is to hold the signal very briefly to allow enough time for the atriums to empty their blood into the ventricles we don't want the signal to just pass straight through the AV node and come down here to the ventricles and then the ventricles contract too quickly before they're filled up properly with blood so you hold the signal very briefly right here and then the AV node releases the signal and sends it down through what's known as the a uh a bundle which is this area right here and then we get into the light right and left bundle branches and then it branches all the way out these little branches that stem out from your bundles are known as pereni fibers so peni fibers are responsible for making sure that all areas of the ventricular wall are getting the signal so that they can be stimulated and start the contraction now as the contraction happen happens a contraction will start all the way down here at the Apex and it contracts and squeezes back up towards these valves so that we either send Blood Out to the systemic circuit or it goes through this valve and it goes out to the right and the left lungs in the pulmonary circuit now what happens if something were to disrupt your SA node the good thing about autoc conduction and this built-in pathway for sending the signal all the way through the heart is if we um take away the SA node which is the pacemaker your AV node will pick up the slack and it'll start the signal it autoc conducts the only thing about it is the further you go down the the auto conduction or your um cardiac conduction system is your intrinsic rate is going to drop so if we take out the SA node and rely on the AV node your intrinsic rate is going to drop to about 4 40 to 60 beats per minute and then if for some reason we lose the AV node your ventricular cells can pick up the slack and they can stimulate themselves to contract but your intrinsic rate is going to drop to about 20 to 40 beats per minute this allows the heart to work as what's known as a functional sensium so a sensium is known is the word for a mass of cells so something like a tumor would be known a mass of cells and known as a sisum the reason that we call the heart a functional sisum is because it works like one mass of cells we know that the heart is made up of all individual myocardial cells but they're all branched in series so they're all locked in with each other and they simultaneously stimulate each other which allows them to functionally work like one massive cell now we know that the atriums beat ahead of the ventricles so that they can EMP the blood into the ventricles before they contract and the wall of the left ventricle is four to five times thicker than the right ventricle because it has to send blood all the way through the systemic circuit from head to toe across the body whereas the right ventricle has the easy job of just sending blood right here to the right and the left lungs and when we talk about a cardiac cycle so I've mentioned this before a cardiac cycle is a syy and a diast paired together so we get a contraction and then a relaxation and that's one full cardiac cycle at a resting state we spend about 2/3 of the cardiac cycle in diast that's beneficial for us because it allows us to be able to fully fill the ventricles with blood before they contract again to send it out to the systemic circuit now comparing a cardiac cycle from a resting state to heavy exercise if this is an example at rest we have somebody that has a heart rate around 75 beats per minute that would put uh Cy at about 0.3 seconds and dially roughly around half a second so if you do the math there we're spending 23 of the cardiac cycle in diast but if you compare that to heavy exercise say somebody gets their heart rate up to 18 180 beats per minute look at what happens to syy and diast now we're spending more time in consist and if you do that math then we're spending 2/3 of our cardiac cycle in and let's just erase it in syy that's why stroke volume is so important if you already have a higher stroke volume everybody's going to be able to increase their heart rate and you can see now that we're spending more time in syy so we're not giving the the heart enough time to fully fill up before it contracts The ventricle again so if you already have a a a prior increase in stroke volume and your blood isn't high in viscosity then we're allowing the blood to empty faster because it can move faster you've got a larger volume of fluid that can exit the left ventricle with each one of those contractions and Supply the metabolic demand of exercise and the way that we regulate our heart rate is is by a balance between parasympathetic and sympathetic nervous system so at rest these two are in balance with each other so they're kind of counteracting one another they're mainly under parasympathetic control it's really bringing everything down keeping everything regulated because what parasympathetic control by way of the vagus nerve does is it hyperpolarizes your heart tissue so if we draw that here and we have depolarization threshold and then let's say this is our resting membrane potential of cardiac tissue remember type one muscle fibers have a resting membrane potential up here so it's closer to depolarization threshold meaning it's easy to stimulate but with cardiac tissue the vagus nerve releases or causes the release of acetylcholine and acetylcholine drops your resting membrane potential f further away from depolarization threshold so it makes it harder to stimulate since it's harder to stimulate that keeps our heart rate low because it takes an extra strong stimulus to get you up there that parasympathetic control is what's called vagal tone now all of this is at a resting state so what happens when we go into exercise when you start to exercise we start to pull away that vagel tone that parasympathetic atic control and that brings our resting membrane potential closer up to depolarization threshold so again if this was our resting membrane potential at a resting state depolarization threshold here when we start to pull away the vagal tone and the parasympathetic control the resting membrane potential creeps up and it gets closer to depolarization threshold so now the membrane potential only has to travel this far to get stimulated and allows our heart rate to increase at a faster rate now that initial increase going from rest to about 100 beats per minute is simply the withdrawal of the vagal tone when we go above 100 beats per minute that's when we're actually relying on the sympathetic nervous system so the sympathetic nervous system will release norepinephrine so norepinephrine gives us that adrenaline response we start to see spikes in our physiolog variables so what norepinephrine will do is it'll stimulate beta receptors in the heart which leads to an increase in our heart rate and the contractility of the heart or in other words the force of the contraction of your ventricles excuse me so not only are we Contracting at a faster rate but we're also Contracting harder so that we can get more of that blood volume up and out of the ventricles and send it out to the systemic circuit the way that we know a lot of the information that we do about the Heart Is by way of something known as the electrocardiogram maybe you've seen this in a clinical setting or you've seen it on a TV show before the electrocardiogram is often represented by the variable or by the abbreviations ECG or EKG there was a difference between the two and the only difference is electric cardiogram in the English language is spelled with an e or SC there for cardiogram with EKG it comes from down here the guy that developed this technique is William einthoven and will an einthoven einthoven uh in the language spelled it with a K there but what the electrical cardiogram does or what I like to call EKG just because it's easier to say is we use these little surface electrodes across the chest these are called precordial leads so these precordial leads or chest leads are set up in an orientation to pick up the electrical activity of the heart either at a resting state or during a stressful State such as exercise so I'm going to get rid of these circles right here and draw what our heart looks like in our chest cavity so your heart looks like that we like to think that the heart sits up and down like this in my chest cavity but it actually doesn't my heart is tilted a little bit within my chest cavity and the apex of the the heart is pointed down towards my left HP and that's the reason that we have these electrodes oriented in that direction is we're picking up the electrical activity as it leads the SA node and goes to the AV node and then down through theeni fibers in both ventricles what this does is as the electrodes pick up the electrical activity it sends a signal back to a uh computer and a printer and we get this graphical representation of the electrical activity of the heart now what the electrical activity of the heart does is it creates waves on the graphical representation so maybe you've seen a TV show some medical TV show where they had electrodes hooked up to somebody and they're looking at a screen so that they can monitor the electrical activity of the heart and then you see all of the sudden it goes into what's known as a flatline so the Flatline is when you hear that beep across the TV show and they go into all bringing out the paddles and Ste trying to artificially stimulate the heart to restart it and everything what that flat line is called is that's the iso electric line meaning that there's no electrical activity happening in the heart at that time point now what these waves are are these little deflections that represent electrical activity in the heart and they create these deflections away from the iso electric line so we see these waves that look like that and we're going to flip back and for between this slide and the next slide to show what these waves look like and what they represent the first one that you'll see on um a QR or on the electric cardiogram is the p-wave the p-wave represents the atrial depolarization so this is when the signal is traveling from the SA node so it leaves the SA node right here and it travels to the AV node so your signal is traveling down through the atriums right there now remember what's the job of the AV node the AV node is responsible for holding the signal very briefly so we get this little hold right here where we go back to a flatline meaning that at that time Point there's no electrical activity happening so AV no's holding on to it right there and then that gets us to our QRS complex so QRS complex is the time point from when the AV node releases the signal and then we get this big big spike in the deflection or this wave here and all the way to this point right here is when the signal is traveling from the release of the AV node all the way through the ventricles and causing the ventricular depolarization and the contraction to occur and then our last deflection that we have is ventricular repolarization so we go back into this little Flatline for a brief moment and then we have this time point when the ventricles are repolarized Rising so if you remember back in unit two we talked about absolute and relative refractory periods and we have to allow enough time for the membrane to repolarize before we get another signal another action potential can happen so this is that repolarization phase of your myocardial tissue we can also look at an EKG based on intervals so you have the PR interval which is your atrioventricular conduction so if we go back to our slide here this is when SA node starts the signal all the way till AV node is about ready to release the signal there so this is the time point that the signal is spent in your atriums and then we have the QRS interval so the QRS interval is your intraventricular conduction time frame so as soon as the AV node releases a signal and it gets to right here all the way to your s segment or your swave right there this time frame here is the time that the electrical signal is spent in your ventricles and then our last one here is the St interval so the St interval is the length of time that it takes the ventricles to repolarize so we're going from right here on that swave all the way to the end of the t-wave and that time frame is is the repolarization of your ventricular cells after they've gone through depolarization and contraction there's a lot of information you can gather off of an EKG graphical representation so like we said we've got these deflections that shows what's happening in the heart we can look at time intervals we could look at the spike here of the rwa what and what that represents is the magnitude of the signal um that's happening within the cardiac tissue so all kinds of information and during clinical settings if you go into a hospital and work with EKGs or you work in a clinic with EKGs you'll learn a whole lot more there's tons of things that we can do with EKGs and looking at what shape do uh you know our t- waves have so you could have an inverted t-wave you could have an elevated ST segment that represents all kinds of things like myocardial infarctions or eruptions in the cardiac conduction system so here it's showing you the relationship of the electrical events to an EKG so right here where we have that P wve at the beginning that's when the signal is being sent through your atriums down to the AV node we have that brief time point where we hit the iso electric line that's when AV node is holding the signal very briefly and then the big spike up to the r wve we're sending the signal all the way down to the apex of the heart and then during that swaave when it's coming back down that's the completion of ventricular depolarization and we're getting that contraction to happen in sending blood up and out of our ventricles then t-wave is when we start to repolarize so you can see the green area here we're starting at the apex of the heart and we're repolarizing up to the top of the ventricles and then when t-wave is over that means that we've reached the completion of our ventric repolarization and we're ready for the next signal to start at the SA node so we'll start all the way back up here again and get the p-wave to happen and atrial uh depolarization and then ventricular depolarization again you don't necessarily have to know these right now but this is just a brief introduction about an EKG and how it's set up so in EKG what most commonly in a hospital or in a clinic we use something called a 12 lead EKG what that means is we're getting 12 views of the heart however we use 10 electrodes to do that so you have the right arm the left arm the right leg and the left leg which generally you're going to put those down there on the hips and then uh like we said these are your limb leads those right arm left arm right leg and left leg and then you have six chest leads which are called precordial leads and that's V1 through V6 V1 through V6 have definite U anatomical locations here so V1 we're going to place is the only one of the V leads of the chest leads that goes on the right side of the body and it's at the fourth intercostal space so easiest way to do that is find the clavicle and then you're going to try and kind of push down on the chest and you feel these little soft spaces so that's going to you're going to come down to that forc soft space in between The Ridges of your ribs and that's going to be where V1 goes in general that's going to be somewhere right here around the middle of the chest then we're going to hop over and we're going to go to V2 V2 is directly on the other side of the sternum at the fourth intercostal space on the left side of the sternum and then we going to skip V3 so let's do this let's skip V3 and we're going to go to V4 the reason for that is because you'll notice V3 doesn't have a defined anat anatomical location whereas V4 does so we're going to go to V4 which is the mid clavicular line the middle of your clavicle here and we're coming straight down to the fifth intercostal space now we can come back to V3 and we're going to put V3 directly in between V2 and V4 then we go V5 five so the order let's write this the order of putting these on is one two 3 four and then we're going to come to V5 and do V6 so V5 is on the anterior auxilary line same level as V4 which is your fifth intercostal space so the anterior axillary line is right through here easiest way to explain where that is is if you put your arm by your side and find the crease of your your armpit you're going to come straight down the side of the body to that fifth intercostal space there and then the last one that we put on is V6 so V6 is the mid mid axillary line at the same level of V4 and V5 so what we can do here is we can lift the arm up find the middle of the armpit and come straight down the midline of the body to that fifth intercostal space there now if our heart is sitting in here what we end up see seeing as our heart is pointed down towards our left hip so all of these leads are giving us these different views of the heart both from The Atrium the ventricles we're looking at lateral and medial views we're looking at anterior and posterior views of the heart and so on when you get your EKG print out it looks like this and all EKG printers and papers are standardized so that we can measure magnitudes of signals and we can measure things like heart rate so the printer feeds at a rate of 25 mm per second each one of these 1 millimet squares right here represents 0.04 seconds and the large squares which is made up of five small squares you can see the bolded lines here represent a large Square that's 0.2 seconds so as that printer paper uh or EKG paper is feeding through the printer what we can do is we can Mark where did the ventricular depolarization happen and let's say the next one happens right here we can count the number of boxes in between our R waves representing the ventricular contraction and we can determine heart rate from that so what you can do is you can measure the number of large boxes between two consecutive r waves two consecutive spikes on the EKG and divide 300 by the number of large boxes or if you want to be as specific or as accurate as possible we'd measure the number of small boxes in between two consecutive rways and divide 1,500 by the number of small boxes so here's an example we don't have to do this right now but you can come back to these slides and actually do this on your own easiest way I'll tell you to do this is find the r waves if possible that fall on a line when you get a r wve like this it's kind of in between uh two lines there it makes it a little bit more difficult but if we can use our waves that fall on a line then we can be as accurate as possible so we can see this one's here on a line and this one's here on a line so what we can do is we could either count the number of small boxes and say that this is roughly one two three that's about 34 plus another quarter so really almost four large boxes there or like we said be as specific as possible and count the number of small boxes here in between two consecutive rways I'm just trying to draw dots and this is a mess but two consecutive rways there and divide the 1500 by the number of small boxes and then the last little bit this is not information that you have that you'll be tested on this is Advanced EKG stuff but these are some disruptions that you may see in an EKG if we go back one slide this is what sinus rhythm or normal Rhythm should look like in the clinical world this is what we would call sinus rhythm meaning normal but when we go back here you can definitely see that there's some disturbances in the electrical conduction here so this is known as a PVC a premature ventricular complex and it's known as a biny PVC so every two every other one we get this premature ventricular contraction so you can see here we have a p wve we have q RS and then we have a t-wave but you'll notice before this QR s there's no P wve meaning that the ventricles just contracted on their own there was a premature contraction that didn't come from the sa note this is trigeminy PVC so every third one so we have one two three premature one two three premature so that's trigeminy PVC quadrin is the same thing every fourth one so one two three four is premature 1 2 3 4 is premature this is known as ventricular fibrillation so you'll notice on there you don't have any identifiable p-wave t-wave this is just kind of this fluttering activity of your ventricles so your ventricular cells are are getting this chaotic signal from their own uh conduction system and it's causing them to go into this fluttering and the contraction rate is very fast this is known as tors de points which is stands for twisting around the point or twisting around the iso El electric line so we drew isoelectric line there you'll notice that we've got big spikes we've got little spikes here and then we've also got down in the negative deflection in that direction so believe it or not this is something that everybody has experienced have you ever felt like your heart skipped a be or you get shocked and you kind of get that fluttering feel deing within your chest cavity that's torsade day points this normally corrects itself so you'll get that skipped bead or you'll kind of get that anxious fluttering feeling in your chest but your heart will reset itself using the SA node and all of this goes away and we'll go back to getting our p-wave our QRS and our t-wave on our EKG now when we have something like this this is known as a bundle branch block so you'll notice here we have the QRS complex comes up and it has this double Peak on it that's known as a by modal Peak on the QRS so you'll hear sometimes people refer to this in a clinical setting as bunny ears on the QRS complex so when you get bunny ears on the QRS complex what's happening is Av node remember AV node released the signal right here and the signal went down through your ventricles but as it gets down into your ventricles the bundle branch block exactly what it's saying there is the bundle branch is blocking the signal it's holding on to it very briefly and then it releases it and it lets it Go and it goes back down through the rest of your ventricles so we've got the signal starting to go through the ventricles here it stops then it comes back and it releases and it goes through the rest of the ventri and then just a few others these are first degree heart block um which is really just a delay and not truly a block here but what you'll notice is these p uh PR intervals right here are really long so the AV node is holding on to the signal a little bit longer than it should with a second degree type one what we end up seeing here is the p-wave is normal then it gets long then it gets even longer and then all of the sudden the p wve is going to hold on to the signal so long that it's considered a dropped beat meaning that it didn't release the signal down through your ventricles and we didn't get the QRS complex like we should have and then with a second degree type two you just notice that there's a p-wave here and there's no Q Q RS complex P wve there and no QRS complex so it's a missing beat where the AV node is just holding on to the signal third degree heart block we have p waves here and it's not the AV node is not letting go of the signal and allowing it to travel through the QRS complex so in this case the ventricular cells have to stimulate themselves so that they can get the contraction to occur and pump the blood out through the ventricles this goes back to what we were talking about at the very beginning with autoc conduction meaning that it has its own built-in conduction pathway and if all of these Pathways if the SA node and the AV node are knocked out and they're not doing their job like they're supposed to the ventricular cells can pick up the slack and still stimulate the heart to contract but you'll notice the look at the time frame between these ventricular complexes here so that's going to lead to a heart rate that's really really slow it's defin Ely beneficial we can do that but in per say of something like exercise we wouldn't be able to supply the demand of exercise because uh your heart rate can't increase enough to be able to send Blood Out to the systemic circuit for that metabolic demand all right that gets us all the way through this just brief introduction into EKG like I said you won't be tested on this information um for this course but it just gives you an idea of the cardiac conduction system which is something that you do need to know the sa to the AV node AV node holds it the bundle branches then down through the pereni fibers that's something that you do need to know but when it comes to the EKG stuff you don't necessarily need to know that but it's just an introduction for you if you're interested in going into a clinical field and maybe it gives you an idea of things that can happen in a hospital as an exercise physiologist doing cardiac stress testing or in a clinic if you have somebody that's coming in as a cardiac patient so if you have any questions feel free to reach out to me but our next lecture will be jumping into our respiratory system so we're going to go through a lot of respiratory anatomy and physiology and how everything works the pressured gradients that are present and then we'll get into some adaptations and some specific things like elevation and altitude training and how those things can affect your respiratory physiology

all right we&#39;re going to have a short lecture here just to talk about the cardiac cycle and the conduction pathway how does the signal travel through the heart and then what are the methods and the techniques that we use to be able to look at that and determine what&#39;s going on with the heart both at a resting state and during a state of stress something like exercise this is really important for when we&#39;re talking about the clinical population and understanding how the heart functions so the heart contraction by way of something known as autoc conduction so autoc conduction means that it has its own built-in electrical pathway that allows it to conduct this electrical impulse all the way from the top of the heart down to the apex of the heart so that we can get the heart to contract and work as one unit so there&#39;s no external signal or stimulus that&#39;s required and it starts all the way up in your atriums and sends a signal all the way down through the Atri through the ventricles and it comes back up through the ventricular walls and we start the contraction that squeezes the blood back up and out of the heart now as long as your auto conduction is working appropriately then we end up seeing that our intrinsic rate of our contraction is around 60 to 100 beats per minute remember we&#39;d like to see that somewhere between 60 and 80 but the acceptable range is 60 to 100 now when we look at the cardiac induction system let&#39;s flip to this slide right here the signal starts up here in something known as the sa note so it&#39;s your sinoatrial node and the SA node is also known as the pacemaker of the heart and what that means is it&#39;s the one that&#39;s initiating the signal so it starts a signal and it sends it down here to something known as the atrioventricular node or the AV node and the job of the AV Noe is to hold the signal very briefly to allow enough time for the atriums to empty their blood into the ventricles we don&#39;t want the signal to just pass straight through the AV node and come down here to the ventricles and then the ventricles contract too quickly before they&#39;re filled up properly with blood so you hold the signal very briefly right here and then the AV node releases the signal and sends it down through what&#39;s known as the a uh a bundle which is this area right here and then we get into the light right and left bundle branches and then it branches all the way out these little branches that stem out from your bundles are known as pereni fibers so peni fibers are responsible for making sure that all areas of the ventricular wall are getting the signal so that they can be stimulated and start the contraction now as the contraction happen happens a contraction will start all the way down here at the Apex and it contracts and squeezes back up towards these valves so that we either send Blood Out to the systemic circuit or it goes through this valve and it goes out to the right and the left lungs in the pulmonary circuit now what happens if something were to disrupt your SA node the good thing about autoc conduction and this built-in pathway for sending the signal all the way through the heart is if we um take away the SA node which is the pacemaker your AV node will pick up the slack and it&#39;ll start the signal it autoc conducts the only thing about it is the further you go down the the auto conduction or your um cardiac conduction system is your intrinsic rate is going to drop so if we take out the SA node and rely on the AV node your intrinsic rate is going to drop to about 4 40 to 60 beats per minute and then if for some reason we lose the AV node your ventricular cells can pick up the slack and they can stimulate themselves to contract but your intrinsic rate is going to drop to about 20 to 40 beats per minute this allows the heart to work as what&#39;s known as a functional sensium so a sensium is known is the word for a mass of cells so something like a tumor would be known a mass of cells and known as a sisum the reason that we call the heart a functional sisum is because it works like one mass of cells we know that the heart is made up of all individual myocardial cells but they&#39;re all branched in series so they&#39;re all locked in with each other and they simultaneously stimulate each other which allows them to functionally work like one massive cell now we know that the atriums beat ahead of the ventricles so that they can EMP the blood into the ventricles before they contract and the wall of the left ventricle is four to five times thicker than the right ventricle because it has to send blood all the way through the systemic circuit from head to toe across the body whereas the right ventricle has the easy job of just sending blood right here to the right and the left lungs and when we talk about a cardiac cycle so I&#39;ve mentioned this before a cardiac cycle is a syy and a diast paired together so we get a contraction and then a relaxation and that&#39;s one full cardiac cycle at a resting state we spend about 2/3 of the cardiac cycle in diast that&#39;s beneficial for us because it allows us to be able to fully fill the ventricles with blood before they contract again to send it out to the systemic circuit now comparing a cardiac cycle from a resting state to heavy exercise if this is an example at rest we have somebody that has a heart rate around 75 beats per minute that would put uh Cy at about 0.3 seconds and dially roughly around half a second so if you do the math there we&#39;re spending 23 of the cardiac cycle in diast but if you compare that to heavy exercise say somebody gets their heart rate up to 18 180 beats per minute look at what happens to syy and diast now we&#39;re spending more time in consist and if you do that math then we&#39;re spending 2/3 of our cardiac cycle in and let&#39;s just erase it in syy that&#39;s why stroke volume is so important if you already have a higher stroke volume everybody&#39;s going to be able to increase their heart rate and you can see now that we&#39;re spending more time in syy so we&#39;re not giving the the heart enough time to fully fill up before it contracts The ventricle again so if you already have a a a prior increase in stroke volume and your blood isn&#39;t high in viscosity then we&#39;re allowing the blood to empty faster because it can move faster you&#39;ve got a larger volume of fluid that can exit the left ventricle with each one of those contractions and Supply the metabolic demand of exercise and the way that we regulate our heart rate is is by a balance between parasympathetic and sympathetic nervous system so at rest these two are in balance with each other so they&#39;re kind of counteracting one another they&#39;re mainly under parasympathetic control it&#39;s really bringing everything down keeping everything regulated because what parasympathetic control by way of the vagus nerve does is it hyperpolarizes your heart tissue so if we draw that here and we have depolarization threshold and then let&#39;s say this is our resting membrane potential of cardiac tissue remember type one muscle fibers have a resting membrane potential up here so it&#39;s closer to depolarization threshold meaning it&#39;s easy to stimulate but with cardiac tissue the vagus nerve releases or causes the release of acetylcholine and acetylcholine drops your resting membrane potential f further away from depolarization threshold so it makes it harder to stimulate since it&#39;s harder to stimulate that keeps our heart rate low because it takes an extra strong stimulus to get you up there that parasympathetic control is what&#39;s called vagal tone now all of this is at a resting state so what happens when we go into exercise when you start to exercise we start to pull away that vagel tone that parasympathetic atic control and that brings our resting membrane potential closer up to depolarization threshold so again if this was our resting membrane potential at a resting state depolarization threshold here when we start to pull away the vagal tone and the parasympathetic control the resting membrane potential creeps up and it gets closer to depolarization threshold so now the membrane potential only has to travel this far to get stimulated and allows our heart rate to increase at a faster rate now that initial increase going from rest to about 100 beats per minute is simply the withdrawal of the vagal tone when we go above 100 beats per minute that&#39;s when we&#39;re actually relying on the sympathetic nervous system so the sympathetic nervous system will release norepinephrine so norepinephrine gives us that adrenaline response we start to see spikes in our physiolog variables so what norepinephrine will do is it&#39;ll stimulate beta receptors in the heart which leads to an increase in our heart rate and the contractility of the heart or in other words the force of the contraction of your ventricles excuse me so not only are we Contracting at a faster rate but we&#39;re also Contracting harder so that we can get more of that blood volume up and out of the ventricles and send it out to the systemic circuit the way that we know a lot of the information that we do about the Heart Is by way of something known as the electrocardiogram maybe you&#39;ve seen this in a clinical setting or you&#39;ve seen it on a TV show before the electrocardiogram is often represented by the variable or by the abbreviations ECG or EKG there was a difference between the two and the only difference is electric cardiogram in the English language is spelled with an e or SC there for cardiogram with EKG it comes from down here the guy that developed this technique is William einthoven and will an einthoven einthoven uh in the language spelled it with a K there but what the electrical cardiogram does or what I like to call EKG just because it&#39;s easier to say is we use these little surface electrodes across the chest these are called precordial leads so these precordial leads or chest leads are set up in an orientation to pick up the electrical activity of the heart either at a resting state or during a stressful State such as exercise so I&#39;m going to get rid of these circles right here and draw what our heart looks like in our chest cavity so your heart looks like that we like to think that the heart sits up and down like this in my chest cavity but it actually doesn&#39;t my heart is tilted a little bit within my chest cavity and the apex of the the heart is pointed down towards my left HP and that&#39;s the reason that we have these electrodes oriented in that direction is we&#39;re picking up the electrical activity as it leads the SA node and goes to the AV node and then down through theeni fibers in both ventricles what this does is as the electrodes pick up the electrical activity it sends a signal back to a uh computer and a printer and we get this graphical representation of the electrical activity of the heart now what the electrical activity of the heart does is it creates waves on the graphical representation so maybe you&#39;ve seen a TV show some medical TV show where they had electrodes hooked up to somebody and they&#39;re looking at a screen so that they can monitor the electrical activity of the heart and then you see all of the sudden it goes into what&#39;s known as a flatline so the Flatline is when you hear that beep across the TV show and they go into all bringing out the paddles and Ste trying to artificially stimulate the heart to restart it and everything what that flat line is called is that&#39;s the iso electric line meaning that there&#39;s no electrical activity happening in the heart at that time point now what these waves are are these little deflections that represent electrical activity in the heart and they create these deflections away from the iso electric line so we see these waves that look like that and we&#39;re going to flip back and for between this slide and the next slide to show what these waves look like and what they represent the first one that you&#39;ll see on um a QR or on the electric cardiogram is the p-wave the p-wave represents the atrial depolarization so this is when the signal is traveling from the SA node so it leaves the SA node right here and it travels to the AV node so your signal is traveling down through the atriums right there now remember what&#39;s the job of the AV node the AV node is responsible for holding the signal very briefly so we get this little hold right here where we go back to a flatline meaning that at that time Point there&#39;s no electrical activity happening so AV no&#39;s holding on to it right there and then that gets us to our QRS complex so QRS complex is the time point from when the AV node releases the signal and then we get this big big spike in the deflection or this wave here and all the way to this point right here is when the signal is traveling from the release of the AV node all the way through the ventricles and causing the ventricular depolarization and the contraction to occur and then our last deflection that we have is ventricular repolarization so we go back into this little Flatline for a brief moment and then we have this time point when the ventricles are repolarized Rising so if you remember back in unit two we talked about absolute and relative refractory periods and we have to allow enough time for the membrane to repolarize before we get another signal another action potential can happen so this is that repolarization phase of your myocardial tissue we can also look at an EKG based on intervals so you have the PR interval which is your atrioventricular conduction so if we go back to our slide here this is when SA node starts the signal all the way till AV node is about ready to release the signal there so this is the time point that the signal is spent in your atriums and then we have the QRS interval so the QRS interval is your intraventricular conduction time frame so as soon as the AV node releases a signal and it gets to right here all the way to your s segment or your swave right there this time frame here is the time that the electrical signal is spent in your ventricles and then our last one here is the St interval so the St interval is the length of time that it takes the ventricles to repolarize so we&#39;re going from right here on that swave all the way to the end of the t-wave and that time frame is is the repolarization of your ventricular cells after they&#39;ve gone through depolarization and contraction there&#39;s a lot of information you can gather off of an EKG graphical representation so like we said we&#39;ve got these deflections that shows what&#39;s happening in the heart we can look at time intervals we could look at the spike here of the rwa what and what that represents is the magnitude of the signal um that&#39;s happening within the cardiac tissue so all kinds of information and during clinical settings if you go into a hospital and work with EKGs or you work in a clinic with EKGs you&#39;ll learn a whole lot more there&#39;s tons of things that we can do with EKGs and looking at what shape do uh you know our t- waves have so you could have an inverted t-wave you could have an elevated ST segment that represents all kinds of things like myocardial infarctions or eruptions in the cardiac conduction system so here it&#39;s showing you the relationship of the electrical events to an EKG so right here where we have that P wve at the beginning that&#39;s when the signal is being sent through your atriums down to the AV node we have that brief time point where we hit the iso electric line that&#39;s when AV node is holding the signal very briefly and then the big spike up to the r wve we&#39;re sending the signal all the way down to the apex of the heart and then during that swaave when it&#39;s coming back down that&#39;s the completion of ventricular depolarization and we&#39;re getting that contraction to happen in sending blood up and out of our ventricles then t-wave is when we start to repolarize so you can see the green area here we&#39;re starting at the apex of the heart and we&#39;re repolarizing up to the top of the ventricles and then when t-wave is over that means that we&#39;ve reached the completion of our ventric repolarization and we&#39;re ready for the next signal to start at the SA node so we&#39;ll start all the way back up here again and get the p-wave to happen and atrial uh depolarization and then ventricular depolarization again you don&#39;t necessarily have to know these right now but this is just a brief introduction about an EKG and how it&#39;s set up so in EKG what most commonly in a hospital or in a clinic we use something called a 12 lead EKG what that means is we&#39;re getting 12 views of the heart however we use 10 electrodes to do that so you have the right arm the left arm the right leg and the left leg which generally you&#39;re going to put those down there on the hips and then uh like we said these are your limb leads those right arm left arm right leg and left leg and then you have six chest leads which are called precordial leads and that&#39;s V1 through V6 V1 through V6 have definite U anatomical locations here so V1 we&#39;re going to place is the only one of the V leads of the chest leads that goes on the right side of the body and it&#39;s at the fourth intercostal space so easiest way to do that is find the clavicle and then you&#39;re going to try and kind of push down on the chest and you feel these little soft spaces so that&#39;s going to you&#39;re going to come down to that forc soft space in between The Ridges of your ribs and that&#39;s going to be where V1 goes in general that&#39;s going to be somewhere right here around the middle of the chest then we&#39;re going to hop over and we&#39;re going to go to V2 V2 is directly on the other side of the sternum at the fourth intercostal space on the left side of the sternum and then we going to skip V3 so let&#39;s do this let&#39;s skip V3 and we&#39;re going to go to V4 the reason for that is because you&#39;ll notice V3 doesn&#39;t have a defined anat anatomical location whereas V4 does so we&#39;re going to go to V4 which is the mid clavicular line the middle of your clavicle here and we&#39;re coming straight down to the fifth intercostal space now we can come back to V3 and we&#39;re going to put V3 directly in between V2 and V4 then we go V5 five so the order let&#39;s write this the order of putting these on is one two 3 four and then we&#39;re going to come to V5 and do V6 so V5 is on the anterior auxilary line same level as V4 which is your fifth intercostal space so the anterior axillary line is right through here easiest way to explain where that is is if you put your arm by your side and find the crease of your your armpit you&#39;re going to come straight down the side of the body to that fifth intercostal space there and then the last one that we put on is V6 so V6 is the mid mid axillary line at the same level of V4 and V5 so what we can do here is we can lift the arm up find the middle of the armpit and come straight down the midline of the body to that fifth intercostal space there now if our heart is sitting in here what we end up see seeing as our heart is pointed down towards our left hip so all of these leads are giving us these different views of the heart both from The Atrium the ventricles we&#39;re looking at lateral and medial views we&#39;re looking at anterior and posterior views of the heart and so on when you get your EKG print out it looks like this and all EKG printers and papers are standardized so that we can measure magnitudes of signals and we can measure things like heart rate so the printer feeds at a rate of 25 mm per second each one of these 1 millimet squares right here represents 0.04 seconds and the large squares which is made up of five small squares you can see the bolded lines here represent a large Square that&#39;s 0.2 seconds so as that printer paper uh or EKG paper is feeding through the printer what we can do is we can Mark where did the ventricular depolarization happen and let&#39;s say the next one happens right here we can count the number of boxes in between our R waves representing the ventricular contraction and we can determine heart rate from that so what you can do is you can measure the number of large boxes between two consecutive r waves two consecutive spikes on the EKG and divide 300 by the number of large boxes or if you want to be as specific or as accurate as possible we&#39;d measure the number of small boxes in between two consecutive rways and divide 1,500 by the number of small boxes so here&#39;s an example we don&#39;t have to do this right now but you can come back to these slides and actually do this on your own easiest way I&#39;ll tell you to do this is find the r waves if possible that fall on a line when you get a r wve like this it&#39;s kind of in between uh two lines there it makes it a little bit more difficult but if we can use our waves that fall on a line then we can be as accurate as possible so we can see this one&#39;s here on a line and this one&#39;s here on a line so what we can do is we could either count the number of small boxes and say that this is roughly one two three that&#39;s about 34 plus another quarter so really almost four large boxes there or like we said be as specific as possible and count the number of small boxes here in between two consecutive rways I&#39;m just trying to draw dots and this is a mess but two consecutive rways there and divide the 1500 by the number of small boxes and then the last little bit this is not information that you have that you&#39;ll be tested on this is Advanced EKG stuff but these are some disruptions that you may see in an EKG if we go back one slide this is what sinus rhythm or normal Rhythm should look like in the clinical world this is what we would call sinus rhythm meaning normal but when we go back here you can definitely see that there&#39;s some disturbances in the electrical conduction here so this is known as a PVC a premature ventricular complex and it&#39;s known as a biny PVC so every two every other one we get this premature ventricular contraction so you can see here we have a p wve we have q RS and then we have a t-wave but you&#39;ll notice before this QR s there&#39;s no P wve meaning that the ventricles just contracted on their own there was a premature contraction that didn&#39;t come from the sa note this is trigeminy PVC so every third one so we have one two three premature one two three premature so that&#39;s trigeminy PVC quadrin is the same thing every fourth one so one two three four is premature 1 2 3 4 is premature this is known as ventricular fibrillation so you&#39;ll notice on there you don&#39;t have any identifiable p-wave t-wave this is just kind of this fluttering activity of your ventricles so your ventricular cells are are getting this chaotic signal from their own uh conduction system and it&#39;s causing them to go into this fluttering and the contraction rate is very fast this is known as tors de points which is stands for twisting around the point or twisting around the iso El electric line so we drew isoelectric line there you&#39;ll notice that we&#39;ve got big spikes we&#39;ve got little spikes here and then we&#39;ve also got down in the negative deflection in that direction so believe it or not this is something that everybody has experienced have you ever felt like your heart skipped a be or you get shocked and you kind of get that fluttering feel deing within your chest cavity that&#39;s torsade day points this normally corrects itself so you&#39;ll get that skipped bead or you&#39;ll kind of get that anxious fluttering feeling in your chest but your heart will reset itself using the SA node and all of this goes away and we&#39;ll go back to getting our p-wave our QRS and our t-wave on our EKG now when we have something like this this is known as a bundle branch block so you&#39;ll notice here we have the QRS complex comes up and it has this double Peak on it that&#39;s known as a by modal Peak on the QRS so you&#39;ll hear sometimes people refer to this in a clinical setting as bunny ears on the QRS complex so when you get bunny ears on the QRS complex what&#39;s happening is Av node remember AV node released the signal right here and the signal went down through your ventricles but as it gets down into your ventricles the bundle branch block exactly what it&#39;s saying there is the bundle branch is blocking the signal it&#39;s holding on to it very briefly and then it releases it and it lets it Go and it goes back down through the rest of your ventricles so we&#39;ve got the signal starting to go through the ventricles here it stops then it comes back and it releases and it goes through the rest of the ventri and then just a few others these are first degree heart block um which is really just a delay and not truly a block here but what you&#39;ll notice is these p uh PR intervals right here are really long so the AV node is holding on to the signal a little bit longer than it should with a second degree type one what we end up seeing here is the p-wave is normal then it gets long then it gets even longer and then all of the sudden the p wve is going to hold on to the signal so long that it&#39;s considered a dropped beat meaning that it didn&#39;t release the signal down through your ventricles and we didn&#39;t get the QRS complex like we should have and then with a second degree type two you just notice that there&#39;s a p-wave here and there&#39;s no Q Q RS complex P wve there and no QRS complex so it&#39;s a missing beat where the AV node is just holding on to the signal third degree heart block we have p waves here and it&#39;s not the AV node is not letting go of the signal and allowing it to travel through the QRS complex so in this case the ventricular cells have to stimulate themselves so that they can get the contraction to occur and pump the blood out through the ventricles this goes back to what we were talking about at the very beginning with autoc conduction meaning that it has its own built-in conduction pathway and if all of these Pathways if the SA node and the AV node are knocked out and they&#39;re not doing their job like they&#39;re supposed to the ventricular cells can pick up the slack and still stimulate the heart to contract but you&#39;ll notice the look at the time frame between these ventricular complexes here so that&#39;s going to lead to a heart rate that&#39;s really really slow it&#39;s defin Ely beneficial we can do that but in per say of something like exercise we wouldn&#39;t be able to supply the demand of exercise because uh your heart rate can&#39;t increase enough to be able to send Blood Out to the systemic circuit for that metabolic demand all right that gets us all the way through this just brief introduction into EKG like I said you won&#39;t be tested on this information um for this course but it just gives you an idea of the cardiac conduction system which is something that you do need to know the sa to the AV node AV node holds it the bundle branches then down through the pereni fibers that&#39;s something that you do need to know but when it comes to the EKG stuff you don&#39;t necessarily need to know that but it&#39;s just an introduction for you if you&#39;re interested in going into a clinical field and maybe it gives you an idea of things that can happen in a hospital as an exercise physiologist doing cardiac stress testing or in a clinic if you have somebody that&#39;s coming in as a cardiac patient so if you have any questions feel free to reach out to me but our next lecture will be jumping into our respiratory system so we&#39;re going to go through a lot of respiratory anatomy and physiology and how everything works the pressured gradients that are present and then we&#39;ll get into some adaptations and some specific things like elevation and altitude training and how those things can affect your respiratory physiology

Transcript for:Cardiac Cycle and Conduction Pathway

Transcript for:
Cardiac Cycle and Conduction Pathway