ation over to discussing stroke volume stroke volume is defined as the volume of blood ejected from The ventricle during one contraction so if we look at our pressure volume Loop or Wicker's diagram we can demonstrate stroke volume on these graphs stroke volume is the IND diastolic volume which is the amount of blood filling The ventricle at the end of relaxation minus the ins systolic volume which is the amount of blood left in The ventricle after contraction so on looking at our pressure volume Loop the IND diastolic volume is going to be represented here at the end of ventricular filling and it would be the same volume at the end of isov volumetric ventricular contraction on our wiggers diagram the IND diastolic volume is depicted at this point here in systolic volume is the amount of blood in the ventric after it is ejected so this would be our ins systolic volume and this would be the same volume down here and on our wigers diagram the ins systolic volume would be depicted by this volume here so we can calculate the stroke volume by subtracting this number from that number okay or subtracting our in systolic volume from our in diastolic volume so let's look into to see what kind of things might affect stroke volume so this slide takes us back to our discussion of skeletal muscle and you'll recur with skeletal muscle we talked about one of the things that can affect the force of contraction is the sarom length prior to stimulation and what we said is is that within our body our skeletal muscles are arranged in such a manner that they typically are around their optimal length and therefore when we contract a skeletal muscle we're typically getting somewhere around 100% maximum tension now we're going to focus on just the very top part of this graph this portion right here so this next slide zooms into that point and this again represents our skeletal muscle contraction where for the most part we're going to be getting around maximum tension every time we stimulate a skeletal muscle but the cardiac muscle curve looks different the cardiac muscle curve looks like this and so what this demonstrates to us is that around this optimal length and skeletal muscle we're typically Contracting at a very high degree of tension but with cardiac muscle we actually see a much greater range of tension that may be created and this is a normal range of tension that may be created under normal physiologic circumstances so what we're going to do is we're going to adjust this graph somewhat to make it more useful for us with regards to evaluating cardiac function so what we're going to do is is we're going to take the top part of this graph and we're going to stretch this out we're also going to change the names of the X and Y AIS so on the y- AIS we say that that represents maximum tension created and that's really a reflection of the strength of contraction but a more useful term clinically correlating to the strength of contraction would be the actual blood that's ejected with a contraction so we're going to label our y- AIS stroke volume the xaxis represents sarir length prior to stimulation and the length of the sarum ears in the heart is going to be dictated by the amount of blood that's returning to the heart it's going to be the amount of blood that's in that ventricle prior to stimulation and that is the indolic volume so now we have access labels that really are much more useful clinically indolic volume and how it relates to stroke volume so this is going to give us what's referred to as a cardiac function curve so we've polished that curve up and demonstrate again our indolic volume and our stroke volume and this is our cardiac function curve or a length tension curve so the amount of blood that fills the ventricle is going to determine where we are on this x axis so in this particular case if we have uh the amount of blood Return Of The ventricle represented by these rather thin arrows let's say that that gives us a relatively low left ventricular in diastolic volume and in this case that would create a stroke volume of this magnitude but if we increase the amount of blood that returned that would give us a larger indolic volume and this would give us a larger stroke volume and we we can continue to show the relationship between an increase in IND diastolic volume and stroke volume this increase in stroke volume as a result of an indolic volume this relationship was given the name the Frank Starling mechanism so this is an intrinsic property of the heart and what was found out was that in a healthy heart whatever blood that we return to the heart with the next heartbeat that blood will be ejected so we refer to this as shifting to the right along the cardiac function curve so one of the theories behind why this is the why this works this way is that this stretched muscle appears to have caused tronent to have an increased affinity for calcium and with that we get more cross Bridges exposed and therefore can create more tension so this is how stroke volume may be affected by an intrinsic mechanism and we call this the Frank Starling mechanism now there's another way that we can also affect stroke volume and this is going to be related to the sympathetic system and the myocardial contraction this depicts a standard myocardial contraction representing over time how much tension a cardiac myosite May create so if we use this as our normal then what we can show is what happens if we stimulate that ventricular muscle with sympathetic stimulation and I refer you back to our previous picture where this shows sympathetics inating both the sa and the AV node but sympathetics also go and inate the ventricular muscle so it's this activity here that we're going to be depicting on this picture so with sympathetic stimulation we'll see that we not only do we create a more forceful contraction of the ventricular muscle but it also happens more rapidly so this increase in contraction brought about by sympathetic stimulation we refer to this as an increase in contractility so if all other for factors remain constant the more forceful contraction results in a greater stroke volume now we if you recall when we talked about the sympathetic and parasympathetic effects on the SA node we call those chronotropic effects so that's affecting the heart rate here where we're talking about sympathetic stimulation of the ventricular muscle we can refer to those as inotropic effects and this is an extrinsic effect so this is something outside the heart that's impacting the force of contraction now we can show this inotropic effect on our cardiac function curve so recall that contractility this positive onrop effect reflects the change in the force of contraction at the same IND diastolic volume so if this was our indolic volume this would give us this degree of stroke volume due to Frank Starling but if we sympathetically stimulate that ventricular muscle what this results in is an Essence it causes the entire cardiac function curve to rotate upward so at the same indolic volume with sympathetic stimulation we would actually be jumping up this cardiac function curve and that results in a greater stroke volume now recall that our autonomic nervous system uh is on at all times with regards to its Target tissue so we may not only increase sympathetic stimulation but we may also see situations where we can decrease sympathetic stimulation and if we decrease the sympathetic stimulation we would see this curve shifting downwards so this would reflect a decrease in contractility The receptors once again that are activated or that come into play with this inotropic effect are beta 1 receptors on the ventricular muscle so let's try and put a few of these Concepts together here is our starting in diastolic volume and this would reflect an increase in contractility by shifting up the curve so this would be the effect of sympathetic stimulation of beta 1 receptors so an increase in stroke volume as a result of sympathetic stimulation and notice that we're depicting that at the same indolic volume this reflects an increase in indolic volume and this is reflecting an increased stroke volume and this is the Frank Starling mechanism so this change in stroke volume here reflects an increase in stroke volume due to the Frank Starling mechanism this increase in stroke volume represents an increase in stroke volume due to an increase in contractility what we'll see as we continue to move through this section is that often times we're going to see both of these effects at the same time so we may see an increase in IND diastolic volume and an increase in sympathetic stimulation so we see the combined effects of an increased in stroke volume due to Frank Sterling combined with the increased effects due to increased sympathetic stimulation now we can demonstrate this increased contractility uh by a particular descriptive phrase or number let's look at some volumes here let's say we start out with an indolic volume of 145 ML and an insc systolic volume of 65 mlit this would give us a calculated stroke volume of 80 Mill if we increase contractility if we have this positive inotropic effect by sympathetic stimulation what we're going to see is is we still start off at the same IND diastolic volume remember that's how we uh discuss contractility is the effect at the same and diastolic volume so when we stimulate this ventrical beta 1 receptors that causes a more forceful contraction and that's going to eject more blood from The ventricle so we're going to have a lower in systolic volume and this would give us a stroke volume of 90 ml compared to our normal of 80 well the way that we can depict this is with a number number called the ejection fraction so the ejection fraction is a measure of contractility and the way this is calculated is we we calculate the ejection fraction by taking the stroke volume and dividing it by the IND diastolic volume so in this particular case stroke volume divided by indolic volume would give us a con an ejection fraction of 55% in this case where we have sympathetic simulation it would be stroke volume 90 / 145 and that would give us an ejection fraction of 62% so what we're depicting here is an increased ejection fraction which reflects an increase in contractility which is due to sympathetic stimulation or a positive inotropic effect now we've mentioned here that a normal ejection fraction is around 55% um and so these numbers reflect a potential change with that so in summary stroke volume is the amount of blood ejected with a single contraction we can modulate or we can adjust stroke volume by two main mechanisms one is by sympathetic stimulation by beta 1 receptors this would be our positive inotropic effect that results in an increase in contractility or an increased ejection fraction the second mechanism is by changing the in diastolic volume and this is our Frank Starling mechanism