 and welcome to Nursing School Explained. Today I will cover some basic concepts that apply to cardiac physiology. If you haven't already watched the videos on acute coronary syndrome or heart failure or the medications that pertain to those two, please go ahead and watch those as well. This video will give you a brief understanding of how the medications related to the disease process and we'll start by looking at this very basic formula here. So cardiac output equals heart rate times stroke value. What does that really mean? So cardiac output is the amount of blood that is pumped per minute. Well the heart rate is the number of beats per minute and the stroke value is the amount of blood pumped with each beat. So the amount of blood pumped with each beat times the number of beats per minute gives us the amount of blood that is pumped every minute throughout the body. Now the stroke volume, which is the amount that's being pumped per beat, depends on certain factors and those are preload, contractility and afterload. So let's look at those in a little bit more detail. Preload is the volume of blood in the ventricles before the next contraction and there is something that applies called the Frank Starling Law and what that means is the higher the stretch of the cardiac fibers, the higher the force of contraction. The way I like to think about this, about is think about a balloon. So you blow the balloon up with air and the fibers of the balloon they stretch. The more you inflate the balloon when you let it go, the more the higher the contraction or the faster the balloon will deflate because you've completely stretched the fibers. So the fibers stretch, the more that they stretch, the bigger the force of the contraction is. And in the same way that really also pertains to the cardiac muscle fibers, the greater that they stretch, the greater they are able to contract and the greater the cardiac output will be. Now preload determines the amount of the stretch and conditions that increase the preload are hypertension and heart failure. So what does that mean? Now hypertension a lot of times is caused by fluid volume excess. So that's mostly caused by poor dietary choices which is a high sodium diet which will make the patient retain more water. Therefore there will be more fluid volume in the patient's circulatory system that will have to be pumped around. Now that excess fluid volume influences the patient's preload. So again the more volume we have on board, the more stretch we create and then the higher the force of contraction. Now how does that lead to heart failure? Think about it. The more you inflate this balloon and let it go, you inflate it, you let it go and that pertains to the cardiac muscle with every bead. And the more you do it and the harder it has to work, eventually these fibers of the balloon they will kind of get weaker. Think about a rubber band that you stretched. The more you stretch it, eventually it will kind of get floppy. So the same thing happens with the cardiac muscle. So the cardiac muscle cells they will kind of wear around over time and then that heart is not really able to contract because that frame-stirling law, the increase stretch of the cardiac fibers do not create the increased form of contraction again anymore because the heart has had to pump so much volume for such a long period of time that the muscle is just giving out. Now the second part here is the contractility. So the contractility is basically the ability of the heart to contract to create that contraction and that is increased by the sympathetic nervous system and also increased contractability. Contractility increases the stroke volume. So the more I can contract, the harder I can contract, the more that output will be, that cardiac output that we talked about over here. Now afterload basically means after the contraction so that pertains to the peripheral vascular resistance or called PVR which is the force of the left ventricle pumps against. So if you think about the heart what comes after the heart is the blood vessels and right away that's the A-orda. So depending on the pliability or the stretchability of the blood vessels, more or less flexible these blood vessels are, the more or less the heart will have to pump to overcome the pressure that's in these blood vessels to be able to produce that cardiac output and perfuse the tissues. Now over time what happens, arteries get calcified and they harden and that means that they are not able to stretch as they would usually because usually cardiac output happens the arteries dilate a little bit and then with every beat they kind of expand and contract. Now if the afterload is the force of the left ventricle has to pump against and for the most part in older people that'll be require more of a contraction to receive that same cardiac output and the profusion to the distal tissues to make sure that we're getting profusion to the body. Now the afterload also depends on the size of the left ventricle and the blood pressure. So if there is something that impairs the size of the left ventricle so now the patient has had a myocardial infarction or some cardiomyopathy where the cardiac muscle is impaired itself and the chamber the left ventricle itself shrinks then that's going to affect the afterload because now the contractability or the chamber size and the blood volume that we're able to squeeze out with every beat is impaired because there's something going on with the myocardium itself and then increased blood pressure increases the workload so if the pressure is higher the heart has to work harder to get the blood out to the body which leads to LVH or left ventricular hypertrophy. So think about it the heart is a muscle just like any other muscle in your body the more you work it the bigger it will get. So if the blood pressure is really high and that heart is constantly contracting against this increased afterload this increase in blood volume that we're having in these stiff arteries the heart is going to have to work extra hard. Over time it will enlarge just like any muscle will but then the heart according to Frank Starling Law will eventually lose this contractability and the force of contraction and it'll kind of be this very weakened muscle that now is not able to create the cardiac output that we're really looking for and that the tissues need. Now over here I've written down the medications so that you can see how they affect and how they pertain to the cardiac output formula over here. So when we're dealing with preload we're dealing with the amount of blood volume and we've talked about fluid volume excess and as you know with fluid volume excess if we want to get rid of some we'll give the patient some diuretics which help them excrete the fluid therefore the fluid volume status will come down which will decrease the preload. Same with the beta blockers. Beta blockers also affect the preload because they help with the contraction. Basal dilators help with the preload because they dilate the blood vessels so now there's less of a preload because more of that blood remains in the systemic circulation and it's not necessarily put back into the right side of the heart and then morphine also has to do with the preload it really helps to lower it down. Now to our second concept here contractility so the joxin the cardiac glycoside increases the force of the contraction and the way it does that it slows down the conduction through the atrial matricula node and therefore the contraction is able to get a little bit more squeeze so it helps with the contractability with the ability of the cardiac muscle fibers to contract it's a very good medication that is used and then beta blockers not only do they affect the beta one adrenergic receptors at heart but they also affect the sympathetic nervous system they cannot lower that down and therefore they affect contractility over here. Now for our afterload when we're talking about peripheral vascular resistance the amount of resistance that the heart has to overcome to pump into the peripheral vasculature it always has to do with blood pressure like we talked about over here increased blood pressure leads to increased workload and therefore left ventricular hypertrophy so in order to ease the afterload we're going to treat the patient's blood pressure and that is accomplished with ACE inhibitors as well as antiotensin receptor blockers and then morphine also helps to decrease the peripheral vascular resistance because the side effect is hypotension. So if you want to know a little bit more about these medications their mechanism of action and also the side effects and nursing care associated with them please watch the separate video where I discuss these medications in more detail also if you need a more of a review about how ACE inhibitors and ARDs pertain to the RAS the renin antiotensin and osteoarthritis system go back and watch that video where I go a little bit more into the details about that. So I hope this has helped you to gain a little bit better understanding of this formula about the cardiac output and stroke volume and how it pertains to preload contractility and afterload. Thank you for watching Nursing School Explained and I'll see you next time.