Cardiovascular Alterations

well hello and welcome to car alterations in cardiovascular function this is module six and what we're going to be discussing here is we'd be talking about first of all the normal cardiac function and some of the review of anatomy and physiology but then we'll also be moving on into our abnormal cardiovascular function and some of the problems we may see in our patients as a result of that abnormal cardiovascular physiology so first of all let's go back and let's just review a little bit of some of the normal anatomy so here is a picture of the heart over on the right hand side and you can see that it's usually contained within the mediastinal space the mediastinal space is this space in the middle of the chest wall so we have the two lungs one on each side then we have this space in the middle now the mediastinal space is actually a separate space so it has its own fashion that covers it and so on and so forth but remember that all of that is contained within the thorax so any changes that are occurring in the lungs that the lungs become overinflated or under inflated etc that's going to affect the mediastinal space and it's going to affect the cardiac function the heart is covered by the pericardium the pericardium is the outermost covering of the heart the pericardium is going to be the covering of the heart that holds it in place so it not only covers the outside of the heart and kind of you know protects the outside of the heart but it also holds the heart in place so it's anchored inside the chest wall and that's going to keep the heart from bouncing around and moving around inside the chest otherwise if we didn't have a pericardium the heart would just kind of bounce around inside that mediastinum that's not a good thing now it's composed of three different layers we have the epicardium which is part of the endocardium and we also have the myocardium as the muscular layer of the heart so we have the pericardium and the outside let's move on in next layer would be the myocardium the myocardium is the muscular layer see the male part so the myocardium is the muscular layer of the heart and that's the part we're mostly concerned about when we're talking about patients who have myocardial infarctions is we're worried about having some dysfunction some damage to that myocardium the epicardium part of the endocardium here is going to be the innermost layer of the heart and the the thing that's important about that is that this inner layer is going to be coming in contact with the blood also that inner layer is the part where we're going to attach some of our structures like the valves inside the heart so very important because if a patient gets into carditis that can lead to valvular dysfunction and that can lead to the patient developing some types of foreign bodies that can be breaking off and moving throughout the bloodstream so again here is a picture of where the heart would be located inside the chest notices a little bit more to the left than it is to the right so we're not directly underneath the sternum we're a little bit over to the left more than we are to the right and take a look at where the ventricle is now in the bottom picture on the left and gives you an idea where the ventricle is between the sternum and the spinal column right above the diaphragm there so we have the diaphragm coming right up and touching on the lower part of the heart okay now some of these things are significant because if we have disorders in our patients so again go up to the uppermost picture and you're looking at the heart there and you see how close proximity those lungs are in fact the lungs are really touching on either side of that heart so if those lungs become overinflated it's going to squeeze the heart now look at the bottom left picture and you see that the diaphragm is touching the ventricle well what happens if your patient has got some kind of abdominal pathology going on pushing up on that diaphragm that's also going to impact the ventricle and then you can see that over on the right hand side is breaking down our inside layers or breaking down our layers of the heart into their different areas so the pericardium money outside the epicardium and the myocardium and then innermost layer the endocardium just as a review here of the vessels of the heart now you're not going to have to know all the detail about all the different vessels of the heart so if you're looking at this and getting a little overwhelmed thinking oh my gosh how am I going to remember all these you're not going to have to remember all of them but you do want to get a feel for where these vessels are coming from and what they're doing so we have our superior vena cava and the inferior vena cava the inferior vena cava is on the left-hand side of the bottom so those are coming together and going into the right side of the heart specifically into the right atria from the right atria then blood is going to be pumped to the right ventricle and then it's going to be pumped out through the pulmonary arteries so you can see it's kind of they've shaded them kind of purplish here in the picture the right coronary arteries and the left pulmonary arteries and it goes to the lungs then it comes back and it goes through the pulmonary veins now those this might be a little bit harder to see on your picture there but if you look right below the pulmonary arteries you see it's labeled pulmonary veins so that's coming back from the heart different ones and coming back to the left side of the hearts going into left atria and then getting pumped to left ventricle and then pumped out to the aorta okay so that's all the circulation that the heart is doing that's the pumping part and what's happening here with all the plumbing now how is the heart getting fed well the heart is being fed by its own vasculature and these vessels originate from the base of the aorta so at the base of the aorta there are these little vessels that come out and they will feed the heart directly they're broken down here into the right coronary artery the left coronary artery the other one that you often hear about frequently is the circumflex artery and I will see the circumflex listed here on this picture but that's one of the other major coronary arteries that you're going to hear about so those are just some of the major ones notice the right coronary artery is supplying the right side of the heart now that makes sense right left coronary artery supplying the left side of the heart okay that makes sense too now when we look at the coronary vasculature this gives you a little bit more detail just about the coronary vasculature we're not getting into so much detail about some of those other vessels but notice your vessels again so the right corner artery let's go over the left picture of the left picture showing the arteries in the right picture showing the veins so the right coronary artery coming down the right side of the heart and it's going down the right side around the right side and actually going down to the bottom of the heart somewhat so we have not only the right side of the heart being perfused by the right coronary artery but we also have a little bit of the base a little bit of the bottom of the heart that is also being perfused by the right coronary artery this means if there was a blockage in that right coronary artery the patient would right ventricular infarct and/or an inferior wall infarct the inferior wall being the bottom wall inferior bottom wall of the heart now over on the left-hand side we have a couple major vessels here that are important we have the left coronary artery and that's supplying the left side of the heart so very important vessel okay because it's supplying the big pumping chamber of the heart which is the left side of the heart we also have the circumflex artery that comes off now the circumflex kind of comes off and it kind of wraps around so it's more of a circular circumflex so think of circles so it's coming off and it's going around more than it's going down so the right coronary arteries going down the right side left coronary arteries going down the left side circumflex is kind of going around the middle so that might be one way to remember it by thinking of a circle as far as all of these little branches like the anterior interventricular artery and things like that you don't need to get into a lot of detail with those but look at those branches and just see how the entire ventricle is being perfused by that arterial system now if we move over the picture on the right now what we're going to see is here is the heart and it the venous system so now we get the blood there we got to get it back so that's what the venous system is for and the venous system is going to return it the thing that's going to be the problem in most of our patients is not the venous system it's the arterial system and we get a little clot in one of those arteries it blocks the artery it blocks the perfusion to that part of the ventricle and the patient has a myocardial infarction autonomic control of the heart well some of the major things here is going to be the sympathetic and parasympathetic systems so this is the central nervous system that's going to stimulate this the sympathetic nervous system this is your fight-or-flight response epinephrine norepinephrine are released they're going to increase the heart rate and force of contraction now you may have heard terminology before about things like barrel receptors and chemo receptors and the body ok now we're also going to talk about how those baroreceptors and chemo receptors can have two different effects on the heart they can have a effect where they're increasing the heart rate that's called a chrono tropic effect and they can also have an effect where they're increasing the force of contraction and that's going to be called an inotropic effect so going back up to our first one here norepinephrine it increases the heart rate that's chrono tropic think of chrono like a watch or clock chrono tropic and then the force of contraction is I know I you know tropic so those are going to be terms that we might see especially when you get into pharmacology you might see them using that terminology when they're talking about different kinds of medication it's a positive chronic traumatic so positive inotropic med it's talking about the increasing the heart rate increasing the force of contraction okay let's take a look at the parasympathetic system then all right well there needs to be a balance if all we had was sympathetic nervous system everybody would have a heart rate of 180 and we'd have this huge amount of cardiac output in with where our hearts out so there's always this balance between the two it's it's kind of like a seesaw if you have somebody in one end to the seesaw you have to have somebody on the other end of the seesaw or it's not going to be balanced and the same thing happens here with our autonomic controls in the body is we have to have a balance between the sympathetic which is the stimulation part and the parasympathetic which is kind of the relaxation part so the parasympathetic system is going to tell the heart to slow down okay now let's just stop here for a minute and take a look at those two things and think about what happens if they get altered so let's say there's too much sympathetic nervous system stimulation that means the patient would have an increase in our heart rate they'd have tachycardia and then him an increasing force of contraction which means they would have an increase in their cardiac output we're going to talk more about that in other classes about what an increase in 40 cardiac Oppel might look like how about the other side of the coin maybe the patient has too much stimulation of the parasympathetic system well the parasympathetic system is going to decrease the heart rate which means your patient could develop bradycardia maybe their heart rates down to like 40 because they've had the stimulation of the parasympathetic system so those things are constantly in balance if it's out of balance it's going to lead to an Abbe normal situation in your patient that we are going to have to deal with we're going to have to treat next we have the chemoreceptors we've talked about chemoreceptors in terms of other things in the body like acid-base balance etc those chemoreceptors though are going to cause vasoconstriction or vasodilation of the coronary vessels and of the vessels and the rest of the body in order to be able to accommodate for different kinds of conditions that are happening to bodies so co2 o2 pH those things are going to activate our chemo receptors to cause vasoconstriction or vasodilation and that's going to try to optimize our cardiac output all of these autonomic controls are designed to try to optimize our cardiac output none of them are put in place to try to make things more difficult they're put in place to try to maintain homeostasis all of the time in our patient next we have our baroreceptors for stretch they respond to changes in blood pressure we have baroreceptors in the aortic arch and in the carotid bodies and when we have increases or decreases in blood pressure they sense that and say whoa blood pressure is not what it's supposed to be let's fix this and let's either raise the blood pressure or decrease the blood pressure okay let's stop for a second and think about this if the baroreceptors are responding to stretch and they're going to either increase or decrease the blood pressure what are the baroreceptors stimulating okay now if you said the sympathetic and parasympathetic nervous systems you were correct that's what the baroreceptors are going to be stimulating so you see how these things all kind of fit together all right now as far as our cardiac function goes first thing we're going to take a look at in our cardiac function is going to be the heart sounds now hopefully you've had a chance to get a stethoscope or to borrow a stethoscope from somebody and play around of the stethoscope a little bit because what you want to do is to start listening now to heart sounds and start listening in different people I know you haven't had this in the lab yet but that's okay you can still start listening to heart sounds and get a feel for what the heart sounds like now we're talking about an s-1 and an s2 sound this is the lub dub you hear so when you're listening to somebody's heart what you're going to hear is lub-dub lub-dub lub-dub assuming that they've got normal cardiac function and that they don't have any kind of a heart murmur we're going to hear lub dub lub dub now what you're hearing those two sounds are named s1 and s2 so s1 is the LOB s2 is the dub so we've got lub dub s1 s2 and that's what you're hearing when you're listening to the person's heart sound so start listening to yourself and see if you can hear your heart sounds if you already have your stethoscope if not see if you can borrow one from somebody and start listening to heart sound so you can start hearing what a loved dub what the s1 s2 sounds like a heart murmur is an additional sound and it's caused by having turbulent blood flow through the valves if the patient has a really bad like heart failure for example they may end up having all four sounds okay now we haven't defined those yet but there's more than just s1 s2 those are the normal ones but the abnormal ones are s3 and s4 okay we're going to look at those in just a moment a new murmur after a myocardial infarctions mi is an abbreviation for myocardial infarction our deal infarction is when a patient has decreased perfusion to part of the heart and the heart muscle starts to die but a new murmur after an mi could indicate a papillary rupture those are the little muscles that are holding the valves heart failure or pulmonary edema or maybe all of the above so let's take a listen a look at those heart sounds now as I mentioned before s1 and s2 are the normal heart sounds and what I've done here is we just kind of coordinated them with what you'd see on your EKG so if you are looking at a EKG on your patient at the same time that you were listening to heart sounds you'd see something like this this is kind of what it would look like but at any rate we don't need to do that right now in order to be able to understand heart sounds so we're looking at s1 s2 s1 s2 or s1 and s2 or the normal ones lub-dub lub-dub lub-dub let's talk about where those come from so that you have a better idea as to why you're hearing lub dub s1 and s2 when the heart contracts it starts at the atria so the atria contract before the ventricles contract this is actually kind of a good thing if the atria and ventricles contracted at the same time blood wouldn't go anywhere because it's just pressing against each other so instead the atria contract first and they are going to squirt blood down into the ventricle then the ventricles contract and squirt blood out to the body or to the lungs so this is a good system that we have one step at a time rather than having boom you know both of them happening at the same time so we're going to have the atria contract first then the ventricles contract when I listen to somebody's heart now here lub-dub lub-dub in my mind I'm thinking okay that's the atria contracting and the ventricles contracting but the atria and ventricles when they contract it'll make any noise the noise occurs when the valves close it's like the closing of a door when somebody walks out the door it doesn't make noise but when the door slams behind them it makes the noise and that's what we're hearing when we listen to somebody's heart sounds we're actually hearing the valves closed so the atria contract and then the AV valves closed and we get s the ventricles contract and the aortic and pulmonic valve closed and we get s2 so those are the normal sounds that we're hearing all right well listed here we've got additional sounds let's take a look at the first one which is our s3 now an s3 sound is an abnormal sound we shouldn't have it we should just have the atria contract AV valves closed ventricles contract order can pulmonic valve closed we got our s1 or s2 Boop that we're done but if the patient starts to have some dysfunction we can end up having additional sounds as three being one of them an s3 heart sound occurs because our patient has fluid volume overload so there's too much fluid on board now think about the process of what's happening with the heart atria contract AV valves closed then we get s1 ventricles contract the order and pulmonic valve closed we have s2 so now what's happening in the heart after the ventricles contract the atria are filling so now the atria are filling after s2 the atria are filling and because the patient has fluid volume overload they have too much fluid on board too much fluid is rushing into the heart it's going to make the valves flutter and that causes an s3 sound so because the fluid is rushing into the patient's heart it's going to make the valves flutter and we get an s3 sound now in nursing school they taught us about the terms Kentucky and Tennessee the reason for using these terms is to help to understand the pattern by which we hear these sounds so in terms of the s3 it's supposed to be Kentucky Kentucky Kentucky you know you get that s3 coming right after now I never got these down right so what works better for me is these terms that we're going to use here sloshing in and a stiff wall so let's take a look at s3 first with sloshing in so the pattern is going to be lub-dub lub-dub lub-dub da sloshing in slashing and that's the pattern you hear with an s3 sound okay now we're going to listen to three sound so listen carefully here you might have to turn up the speakers a little bit I amplified it a little bit so hopefully you can hear it but we're listening for the pattern this is not a sound from an actual patient it's computer-generated sound so that you can pick up the pattern of what the sound would sound like okay our next sound is going to be the s4 again s1 s2 are the normal ones so we have the atria contracting AV valves closing we get s1 ventricles contract the aortic and pulmonic valve closed we get us two then what's happening okay the atria fill no problem we don't have enough three so the atria filling then what happens right before s1 remember right before s1 what's happening is that the atria are contracting so the HEA are contracting and they're pushing blood out they're contracting and pushing blood out and that is causing the s4 so in an s4 what's happening is that the patient has a non-compliant ventricle maybe the patient's got something like they had a myocardial infarction so they have a non-compliant ventricle because the ventricles ischemic and that's what's causing the patient to have this sound the atria are pushing blood down to this non-compliant ventricle and that's causing this vibration of the valve and that's causing the s4 so and that's for it's going to sound like two lub dub two lub dub two lub dub two lub dub a stiff wall a stiff wall a stiff wall that's the pattern that you're going to hear with an s4 now let's listen to an s4 this one people often have trouble hearing you have to kind of anticipate the sound because the sound comes right before s1 also keep in mind your s 3 s and s 4 s are going to be softer and lower pitched and the s1 s2 so hopefully you're able to hear that alright let's move on and cardiac output is the amount of blood that is ejected from the ventricle every minute so what we have to do in order to determine how much blood is ejected from the heart in a minute is we have to look at the heart rate because the more times per minute the heart beats the more blood it's going to pump out and we have to look at the volume of blood that was in the ventricle when the ventricle contracted so we have to put those two things together now here is the formula for cardiac output cardiac output his heart rate times stroke volume more math all right well and that's what often gets people here as we say oh boy I'm not going to be able to understand this one because it's more math all right wait it's a really pretty easy concept again the more times per minute the heart beats the our rate the more output we get the more volume that is in the blood with each contraction the more volume we get so hopefully that makes a little bit more sense to you just think about it in terms of that how much volume the heart is pumping times how many times per minute the heart beats that gives us our cardiac output normal is about four to eight liters and again we're talking about per minute so four to eight liters a minute at cardiac index is another value we may look at and that takes the cardiac output so our four to eight liters a minute and we divide that by the patient's body surface area wouldn't it make sense that somebody who's larger would need a higher cardiac output than somebody who's smaller and that's why we use the cardiac index so the question at the bottom says how do we know that somebody has an adequate cardiac output well we're going to have to look for clues in the way that the patient's presenting we're not have to look for clues and whether or not organs are being perfused whether or not their skin is being so we're going to have to be looking for clues in all of those areas to be able to tell us that somebody has an adequate cardiac output cardiac output and systemic vascular resistance are some additional components we're going to consider so we did talk about cardiac output here at the top systemic vascular resistance is the resistance of the blood vessels now specifically here we're talking about the arteries the veins don't put up a whole lot of resistance mostly their function is to get blood back to the heart so that's not such a big deal but the arteries are going to be a big deal they're going to cause as a significant amount of resistance think about it like a hose so you're going to go out and wash your car here in summertime and it's nice and warm out and you're going to get the hose out so you get the hose out and you're ready to wash the car and you turn on the hose and you go over and you start trying to spray your car down and there's hardly any water trickling out of that hose at all you go back and you look and look then there it is the hose is kinked now the same things going to happen in the body if the hose gets kinked if the vasculature gets kinked then we're not going to be able to have good perfusion to the rest of the body in addition what happens when you unkink that hose don't you get this big burst of water that comes down through because it was building up so much pressure behind that kink and the same thing happens to with the heart when we get a lot of resistance in the vasculature it backs up to the heart and puts too much pressure on the heart arterial blood pressure is a function of both the systemic vascular resistance and cardiac output in fact if you break up your blood pressure into two components we have the top number which is the systolic and systolic is a component of cardiac output the bottom number the diastolic is a component of your vascular resistance now you're going to get more into that a little bit later on so I just introducing it here don't get real worked up about it you're going to hear it again pulmonary vascular resistance on the other hand comes from the pulmonary system so this isn't something that is going to have a dramatic effect on your cardiac output in most people however if your patient has got some kind of pulmonary condition some kind of chronic pulmonary condition like COPD or pulmonary fibrosis or anything like that then you may end up having some problems with pulmonary vascular resistance the primary things though they're going to affect cardiac output is going to be the components of cardiac output we'll get to those in a moment and our systemic vascular resistance there we are of course components of cardiac output in order to make cardiac output we have to have fluid coming in and fluid going out and if there's not enough fluid coming in there won't be enough fluid to pump so obviously cardiac output will decrease if we don't have enough fluid coming in in addition though we can also decrease our cardiac output if we have a kinked tube so let's go back and let's take a look at that preload again preload and afterload these are terms that are used when we're describing how much fluid is coming into the heart and how much resistance the heart has to pump against and you know these are just terms that I don't know if they come from physics or where they come from but these are terms we use to describe patients who have problems with their cardiac output and when in relationship to our cardiac output we use these terms we can also think about it in terms of the heart being the pump like an IV pump or any other kind of pump and these other components coming before and after so the preload then would be the load before the pump well the load before the pump is going to be the fluid coming into the pump right so there's no other load coming into the pump other than the fluid so preload is fluid volume it's always going to be fluid volume it's going to be increased as it shows here if the patient has hypervolemia in other words if that patient is too much fluid on board like they have heart failure for example or they have some kind of renal problem where they can't get rid of fluid there would be too much fluid on board and too much fluid will enter into the heart and we'll have an increase in our preload now we can also have what just says here on our picture it just talks about increases we can also have a decrease what if your patient was dehydrated then there wouldn't be enough fluid coming to the pump to be able to run the pump and the patient would have a decrease in preload which then would result in a decrease in cardiac output on the other side we have the after load the after load is the resistance that the heart has to pump against the heart the resistance are a test pump against is going to be the arterial vasculature okay so that's pretty straightforward we have the vasculature just like the hose we talked about before becoming kinked if it becomes kinked it's going to increase the resistance the heart has to pump pounced it's like your hos out there and you can't get any flow on the other end of your hose because the hose is kinked and the other thing that happens of course is that fluid starts backing up and you can see from the picture here it looks like fluid is backing up into that left side of the heart which is going to cause the patient to potentially have some problems with their cardiac output couple calculations here these are things that you probably ought to just start getting used to looking at and kind of filing these away someplace so maybe it's a matter of filing this way in some part of your brain so you can come back to and get to it later so some important calculations that you'll have to keep in mind as you go through your nursing career would be these here nurse the pulse pressure is the first one pulse pressure is the systolic pressure minus the diastolic pressure so if you were to take what would be a normal blood pressure of 120 over 80 the systolic would be the 120 minus the diastolic of 80 that means our pulse pressure is 40 there are situations that occur in your patient where pulse pressures can be abnormal and that's why we're going to be checking our pulse pressure and patients to find out what the pressure is for that particular patient so that's something we can be looking at and we're going to talk more about this as you get into some of your more advanced classes mean arterial pressure is another value and this is one that you're going to see right away in your very first clinical the first time you take vital signs and a patient using one of the automated systems our automated blood pressure cuff machines read mean arterial blood pressures so we do need to have an idea as to what that means the mean arterial pressure is the mean pressure we could think of it as and I hate to mess up the different terminologies here but I think about it as being the average amount of pressure that's in the vasculature I mean it's not quite the same but think about it as being the average amount of blood pressure that's in the vasculature so what we take is we take the systolic blood pressure and then we add to it the diastolic blood pressure times two the reason why the diastolic gets twice the waiting in this equation is because diastolic time is longer than systolic time so think about your heart right now your heart beats and then it rests it beats and then it has a period resting the resting period is twice as long as the beating period therefore we're going to give the resting period the diastolic twice the weight in the equation so we take the diastolic pressure times two plus the systolic and divide the whole thing by three a normal mean arterial pressure is greater than sixty and you know this all depends upon your patient population just kind of store that number away in the back of your head that we want to have a mean arterial pressure of 60 in our patient in some situations we may want that pressure to be higher other situations we may want it to be lower but just kind of think of that now is it kind of hang on to that as being kind of what the normal should be so as we look at some of the different areas of the myocardium first of all we need to talk about the endothelium the endothelium remember is the inside lining the inside lining of your organs is the endothelium in this case here the endothelium is going to be both around or on the inside of the heart and the inside of the blood vessels on the inside of the blood vessels the endothelium is going to be very important because this is the area that can become inflamed and this is the area that can start to produce atlas chaotic disease vascular resistance is another one of our components that's going to affect our cardiac output and it can be affected by a variety of different factors including the amount of pressure that's in the vessel to begin with the amount of resistance we have that will affect our blood flow and the resistance is going to be caused by vasodilation or vasoconstriction now there's two other concepts here that we need to think about a little bit one is laminar flow any other is turbulent flow laminar flow is normal flow through a vessel through a tube would be normal full turbulent flow occurs when we have some kind of partial obstruction to that vessel and it starts making the blood move and a turbulent matter rather than just nice and neatly down the river so think about it like this you've got a river and the boats floating down the nice little sailboat floating down the river the river is just moving right along there's no ripples there's no waves the current is just moving nice and neatly down that river that would be similar to what laminar flow would be like nice and smooth things are moving nicely along there etc okay how about if we have a whole bunch of rocks in that river now as the flows going down we're going to get a lot of turbulence a lot of turbulent flow we're going to see a lot of waves and a lot of whitewater and things like that that's the turbulent thing and we don't want to have turbulence inside the vessels because turbulence is going to stimulate clotting clotting then in turn is going to stimulate your patient to develop a thorough addict disease and maybe even thrombosis or emboli that can cause the patient to have an MI or to have a peripheral venous thrombosis blood pressure is the outward measurement of the all of these components put together so we're going to put all these components together in the vessel and then we're going to measure that by looking at our blood pressure the more flow we have the more resistance we have that's what's talked about here in the bottom so here is a picture showing our laminar and our turbulent flow it's hot picture showing a laminar flow and one of the things that's illustrating here is in the center of that vessel we have the greatest amount of flow we're going to have less flow around the sides because now the blood is touching the vessel wall and that's causing a little resistance and slowing it down just a bit not a lot not horrible but just a little bit okay now let's take a look at the bottom picture and in the bottom picture we have some constriction of that vessel notice that now the blood starts going in all sorts of crazy ways it's kind of circling around and things like that so now we have that turbulent flow problem with turbulent flow is it's going to start activating platelets and start causing clots athelets chronic disease is a chronic disease in the arterial system that can cause a patient eventually to develop thrombi to develop clots in the vessels which can then could cause some kind of damage to organs and this ones were mostly concerned about it's going to be the brain in the heart but we get an abnormal thickening and hardening of the vessel that occurs we think what causes after Scott ik disease to occur is it's sometime earlier in our lifetime we encounter some kind of infection and that scars the vessel just a little bit just a teeny little not a big deal you don't have any symptoms at the time but it's a little bit of scarring and the vessel and then the vessels start to cause an inflammatory process as part of the inflammatory process we get platelets to the area and fibrin and things like that and it starts to form this little plaque now this plaque is going to then cause a little bit of turbulence in the area which is going to cause more clotting and more things to start to stick there overtime this is not something that happens overnight this is something that happens over a period of many many years and there are things that are going to contribute to this and possibly make it more likely that your patient will develop atherosclerosis so it's an abnormal thickening and hardening of the vessels we get these deposits inside the lumen of the vessel that are mostly they call it a fatty streak but this little fatty streak starts there and it starts collecting other things on it like fibrin like platelets etc and then it starts to become harder and as it becomes harder it's going to cause more turbulence and possibly cause a clot the other thing that can happen to is that the plaque could break off so it's a hard little plaque sitting there in the vessel and one day it just cracks and breaks off well that thing is going to go downstream and it's going to stop a smaller vessel downstream which could cause them some kind of damage to the heart to the brain or to some other organ system where that little plaque went to so this picture here is showing some of the injury that can occur and how this is going to affect the patient so at the bottom of the page we're seeing the normal artery here and we see the different layers the artery and then on the right hand side we're seeing the disease the occluded artery and in this case here we've built up quite a bit of the the inside layer of the vessel in order to include that artery so that's going to start to cause this fatty streak of this fibrous plaque which starts to limit the inside size of the vessel decrease the blood fall through that vessel and then we're probably going to see some symptoms in our patient diseases the veins now keep in mind that the veins are going to be a low pressure system in the body they're a low-pressure system and they are thin walled and what the veins are doing is bringing the blood back to the heart so we have into the arteries taking the blood to the tissues of the body the veins bringing it back the primary function of the brain is just to get the blood back to the heart so it's a low pressure system we don't need a lot of pressure in there to do that they're thinner walls and arteries arteries have a much thicker muscular layer to them then then veins do veins do have some muscle to them and that's why if you ever go to the doctor's office and they want to draw blood from you and your veins just kind of disappear okay well they kind of constrict it on down there you scare them and they've got to constrict it on down there and then you can't see them so they do have a muscular layer to them it's just not as big as the muscular layer in the arteries also valves are something the arteries don't have and that's about I should say veins have something that arteries don't happen that's valves valves will help to prevent a retrograde flow so we don't want that flow to go backwards we want the flow to go toward the heart so in which case we need to have valves in there to make sure that the flow is moving toward the heart and that backwards skeletal muscles will help to compress those veins and help to move blood back up to the heart so it's really important your patients getting up and ambulating and moving around so that we're getting compression of those muscles and that's compressing those veins and moving blood back up toward the heart this terminology here deep vein thrombosis now you're going to see this terminology kind of thrown around with another one which is venous thromboembolism and I think in most cases now we have changed our terminology and we're talking about these things as being a venous thromboembolism rather than being a deep vein thrombosis and any rate what's happening with either a DVT or VTE however you want to describe it is that we are going to get a clot in one of those veins and that's going to block the flow backwards and the patient's going to get swelling etc of the elem varicose veins which we saw in our previous diagram let's go back take a look at that again see those veins that are really sticking out there's an arrow there pointing to them and the veins are sticking out and they're all distended and torturous and these are veins that have fluid backed up in them so the valves haven't worked very well blood is starting to back up and it's making the valves or it's making the veins rather distend that's called a varicose vein the problem with varicose veins are twofold one is that we have too much blood that is sitting back there and pooling which could cause clotting okay so that could be problem secondly is that because these veins are pooling blood and they're hyper distended we're stretching that muscular layer a little bit too far and that can lead to the patient developing fragility to that vessel which then it could pop and it could bleed and cause problems another common problem that we see with the veins is chronic venous insufficiency so this is a situation where we have inadequate venous return over a long period of time and they probably do in most cases - varicose veins but can also be because we just have valvular incompetence and we're not getting that blood back up to the heart so the venous blood is kind of sitting there in that extremity and then this can cause the patient to develop venous stasis ulcers remember blood has to be continuously moving through the vascular system it has to go through the artery through the capillary and through the vein and back to the heart it's got to be continuously moving for this torque think of this is like stagnant water so you've got a stream going through the back of your yard and something blocks it up and become stagnant and that stagnant water is going to start to stink okay it's going to start to have problems there because it's not moving a nice moving stream stays nice and clean but when it's become stagnant then it starts to have some problems and the same thing is going to happen here the blood becomes stagnant it's starting to back up and we're not getting rid of those waste products and getting them away from the tissue and so therefore it's going to start to cause some dysfunction of the tissue which will lead to a stasis ulcer in other words damage to the tissue and an ulceration hypertension is a situation where we have an increase in our systemic arterial blood pressure in most cases most hypertension is going to be caused by some kind of renal deficit that the kidneys are kicking in and they're starting to the cause the patient to have more renin on board which is causing some phase of constriction or things like that so we have a sustained increase in our peripheral arterial resistance from arterial vasoconstriction this can cause some serious problems in your patient one is that we're going to start to get some chronic damage to the vasculature probably more importantly as the heart has to try to beat against this the heart has to try to push blood past these hypertensive vessels again think about the hose we have the garden hose out there and you're going to wash your car and somebody kink the hose alright so we're going to build up pressure pressure is going to build up behind it now you unkink the hose and you get the sudden whoosh of water that's coming down the hose and the same kind of thing it wouldn't really happen in the body because we're not on kinking but we're getting that back pressure and that back pressure is going to go back to the heart and it's going to put too much pressure on the heart and it's going to cause left ventricular hypertrophy that's LVH and just toss into that there another term for L for left ventricular hypertrophy for LVH another term for that is cardiac remodelling just kind of tuck that away somewhere in the back of your mind just so that you can kind of revisit it at some point in time okay we're not going to get into a lot of detail with that right now angina angina is chest pain it's caused by an inadequate amount of oxygen getting to the myocardium so we're stressing the heart now the patient's starting to have some chest pain in relationship to not getting enough oxygen of the heart heart failure and this diet this abbreviation you see here CH f stands for congestive heart failure what you're going to find is that we're changing the terminology a little bit on this and rather than calling it congestive because very few people actually have the congestion part we call it heart failure so you're going to see these terms interchangeable you might see it written CHF you might see it written just simply as HF meaning heart failure when you get into your clinical areas you might see in addition CHF meaning chronic heart failure and AHF meaning acute heart failure so just so that you're aware if you start seeing these different terms as you move along myocardial infarction that's an mi myocardial infarction is damage to the myocardium because of a lack of blood flow to an area of the heart aneurysms can occur in the vasculature so the aneurysm is now pouching the vessel strokes can occur in the brain thrombosis we can get blood clots so all sorts of complications can result because of hypertension hypertension is abbreviated as HTN you might see this abbreviated in somebody's chart as being simply HT and so that stands for hypertension there's a basically two different types of hypertension the first type is called primary primary is also called essential hypertension so you may see it written in a patient's chart that the patient has essential hypertension that's primary hypertension almost all of our hypertension is primary in nature no particular thing that's causing it there's a number of things we think may be contributing we may think the sympathetic nervous system Raa is the renin-angiotensin system okay so it's actually renin-angiotensin-aldosterone insulin resistance inflammation lots of things we think may be a contributing factor but most of our hypertension we really don't know what it is that's causing the patient to have hypertension so we're going to treat it kind of symptomatically we're going to give the patient medications they keep the blood pressure down and just watch for other conditions to occur in a patient's body we may have a secondary hypertension as well this is caused by some specific problem that we can put our finger on and say okay it's because the patient has renal fire it's because the patient has adrenal tumor so secondary hypertension is one in which we have a actual diagnosis that we can link it to in some cases that might make it easier to treat in other cases it doesn't like adrenal tumor as well you know unless we're going to take out that adrenal tumor it doesn't make it a whole lot easier to treat than if it was just primary so this picture here is just giving you some idea of where some of these things plug in to cause hypertension our patients are starting at the top of the page we have the genetics in the environment so and you know one of the pieces in our environment that causes people to have hypertension is a high caffeine intake so you know that's part of your environment there so we got a little bit of a genetic predisposition we add some caffeine to that and maybe something else like cigarette smoking or whatever and now we're going to have some dysfunction in our sympathetic nervous system remember again Raa as renin-angiotensin-aldosterone system we're going to start seeing some problems with our natural hormones and etc and those things are going to cause vasoconstriction over on the left hand side we also get insulin resistance as a result here as a possible result in this process and on the right hand side some inflammation those things don't cause hypertension but they do contribute to the process so on the left hand side the insulin resistance will also help our sympathetic nervous system to run an angiotensin aldosterone system and causing vasoconstriction on the right hand side our renin-angiotensin-aldosterone system and our sympathetic nervous system along with inflammation will cause renal salt and water retention those things increase our blood volume whereas on the left hand side the vasoconstriction increases our peripheral resistance so put that all together and what do we get we get sustained hypertension so we have an increase in total volume we have an increase in our vascular resistance okay now if you were to treat this now let's assume that the genetics environment whatever we you know there's nothing there to treat the patient has a genetic predisposition to hypertension you know you can take the things out of the environment take the caffeine out of the environment take the cigarette smoking out in the environment okay we can take those things out but we're still stuck with the situation here where the patient has already got this dysfunction going on let's go down to the bottom of the page here and the bottom the diagram and take a look at what we may be able to treat what we may be able to treat is the increased peripheral resistance so we give the patient a medication that causes vaso violation over on the right-hand side increase blood volume we give the patient a medication that allows them to decrease their total fluid volume such as a diuretic a diuretic helps the patient to be able to lose to release some extra fluid so on board so those are some of the things that we can do to treat a patient who has hypertension we can't necessarily go all the way back to the source and change the genetics we can change the environment that's one of the first things they do if somebody comes in and they've got a high blood pressure reading the very first thing your doctor is going to do is say okay change your diet get exercise stop drinking coffee you know they're going to eliminate those things that they can if the patients still hypertensive at that point then we've manipulated everything we can at the top of the screen we've got to move down to the bottom of the screen to use medications to help to treat it because we don't want the patient to have that hypertension because hypertension has consequences associated with it malignant hypertension is a situation where the patient has a rapidly progressing hypertension with a diastolic pressure generally above 120 okay so you might want to correct this when we consider it to be malignant or we consider it to be an urgent type of a hypertension the diastolic pressure generally is going to be considered to be above a hundred and twenty millimeters of mercury the problem with having a blood pressure that high is there's too much pressure there's too much pressure in the vasculature and it's going to cause vessels to burst it can also cause the patient to have significant problems with cerebral edema etc because of hydrostatic pressures pushing fluid out into the brain orthostatic hypotension on the other hand is a situation where the patient has a low blood pressure and this will be evidenced by the patient's standing or sitting now if you've ever known anybody who maybe became dehydrated for example and they stood up and passed out or somebody who went and they gave blood and they stood up and passed out that's a very good clinical example of what orthostatic hypotension does if you were to stand up quickly the blood pressure drops why well the reason why the blood pressure is going to drop when somebody stands or sits and by the way this happens to everybody all the time the reason why your blood pressure drops is because blood suddenly by gravity gets pulled down into the lower extremities now in most case is you have an intact system and this is specifically the sympathetic nervous system it's going to kick in and it's going to recognize this remember those baroreceptors they recognize this immediately and they send out signals to cause vasoconstriction so that you maintain your volume and the upper part of your body but what if you didn't have enough volume onboard then while you're laying down you may feel fine but as soon as you go to stand up or sit up then blood starts rushing down on the lower extremities and yes you have those compensatory mechanisms but they're not enough that it's not enough because your volume is low and that's why you end up passing out now we are going to test orthostatic hypotension in our patients by taking a blood pressure with them laying down with them sitting up and with them standing up so some of the factors that regulate the blood volume in our patient are going to be the amount of blood in them in the vessels to the blood volume and the vessels ADH remember ADH is going to help the patient to be able to retain water the sympathetic nervous system and that's going to be by the function of the catecholamines constricting our blood vessels and in the renin-angiotensin-aldosterone system you're going to see this abbreviated in a number of different ways previously we saw it abbreviated as RA a in this case here their breathing is RAAS so this is the renin-angiotensin-aldosterone system this system is activated by the kidneys so the kidneys kick in and they're going to activate the system now the kidneys are kind of selfish here they don't really care what the blood pressure is and rest the body they're trying to maintain the blood pressure inside the kidney so the kidney senses that there's a decrease in blood pressure and says hey we need more blood pressure down here and it stimulates renin release renin dickens converted to angiotensin and then angiotensin is going to stimulate the vasculature in order to cause vasoconstriction so this process is being stimulated by the kidney because the kidney wants more pressure it doesn't mean we need more pressure it's just the kidney wants more pressure and so that's how this system starts and this out how the system begins aldosterone is also part of this system it's intertwined in the system I remember aldosterone tells the kidneys to hang on to fluid so the kidneys are recognizing they think there's not enough blood volume on board they think the blood pressure is low because there's not enough blood volume on board when in fact the blood pressure to the kidney could be low because we have a constriction or an obstruction of the vessel going to the kidney so in which case stimulating this renin-angiotensin-aldosterone system would be dysfunctional other factors that affect blood pressure include our natural peptide z' the most common one here that we talk about is called BNP BNP stands for brain natura DIC peptide okay now this may be a little confusing for you right you read this it says brain natura DIC peptide a marker for cardiac disease how can brain naturally peptide be a marker for cardiac disease well the fact is that brain a erotic peptide BMP actually comes from the heart so these natural peptide ZAR coming from the heart there's a BNP there's an A&P there's a cmp and we think there may even be a D or EMP so those are just additional ones out there but the one word we're mostly concerned about that we're looking at the most is our BNP the reason why it's called brain netic peptide is because originally how it was first found was it was cultured in the brains of animals so that's where the B part the brain part comes from they have the opposite effect of ADH and renin-angiotensin-aldosterone system instead of having the patient hang on the fluid and increase blood pressure naturally peptides will cause the patient to get rid of fluid and vasodilate which is a good thing if we have too much fluid on board these are a backup system so we shouldn't need these the kidneys should respond when we have too much fluid on board and get rid of it but if they don't we have this backup system of the naturopath tides which is going to help us to be able to maintain our fluid volume and keep it away from the heart baroreceptors we've talked about those we have stretch receptors in the aorta and the carotid and those are going to help us regulate our blood volume and our blood pressure insulin resistance has a role in vascular injury there's a number of things that can lead to insulin resistance even diet can have a dramatic effect on insulin resistance resistance to insulin causes and athelia injury remember the endothelium is the inside lining of the blood vessel and this can be the beginning of the pathogenesis of hypertension and/or athletic disease neural control of our cardiovascular system okay one of the things that's going to do is going to cause a change in the diameter of the arterioles the arterioles are going to primarily affect how much blood is going to get down through the capillary network it's a reflex control of cardiac output and resistance we have our sympathetic stimulation which is going to stimulate things sympathetic stimulation makes everything this is the fight-or-flight response so you get the tachycardia the hypertension etc parasympathetic does just the opposite so if you can remember one of them then just flip it for the other so if the sympathetic system makes the patient hypertensive and tachycardic the parasympathetic system makes the patient hypotensive and bradycardic the bottom line the brain regulates maze of constriction of vessels in order to be able to maintain our blood pressure okay now you might want to add to that not just the brain but we also have those baroreceptors that can function independently of what the brain is doing an aneurysm is an outpouching of a vessel this is an abnormal thing and what happens is that the inside lining of the blood vessel kind of pops through an area weak area and the muscle it's like a hernia so anybody who's had a hernia known somebody who's had a hernia a hernia is an outpouching where the inside of the abdomen some part of the inside of the abdomen could just be the fascia pops out through the muscle layer because of a weak area in the muscle same thing is happening here with an aneurysm we have the inside lining of the blood vessel popping out through the outside lining of the blood vessel because we have an area of weakness in the muscle some things can contribute to this like a Thirsk erotic disease inflammation hypertension certainly the more there is on the vessel the more likely it is that an aneurysm could form this picture is showing some aneurysms what we're seeing here over on the right-hand side is the heart up at the top and you see the aorta coming down and the two kidneys and that big huge wide thing right up there by the heart is a descending this is actually a dissecting aortic aneurysm so big enormous aneurysm now that that is okay just so you're looking at it and thinking oh my gosh that thing looks you know bigger than the heart that thing is split open so we can see the inside of it all right over on the left-hand side let's take a look at some of these different aneurysms over on the left at the top we have aneurysm that is formed on both sides of the vessel so this would be a situation maybe where we have some kind of damage to the vessel wall maybe it's happening at a bifurcation or a connection or something like that where both sides of the vessel wall could be affected at the same time over on the right at the top we have the fusiform saccular and what that is is just one side that that's bulging out now you can see all three layers of the vessel are involved here so we have a muscular weakness and all three layers just kind of bulge out with that muscular weakness so the muscles weak and the muscles bulging too down on the bottom on the left we're seeing a false aneurysm now a false aneurysm means with it we've got like a hole going through the muscle and we've got a clot on the outside so it's not really an aneurysm it looks like an aneurysm because we've got this cloud on the outside of the vessel that makes it look like the outside of the vessel wall is distended over on the right hand side we have what's called dissecting aneurysm and in a dissecting aneurysm the different layers of the vessels start to pull away from each other so what they're showing here is we have a hole in the inside layer of the vessel and the endothelium which is allowing blood to leak between the layers and form this big outpouching what it's not showing you there in the picture is it goes both ways it doesn't just out pouch but it also pushes the inside layer in and eventually it's going to push the inside layer again enough that there's no blood flow past it peripheral vascular disease is another of our cardiovascular disorders and this is a situation where we don't have enough arterial blood flow getting to our patient so one of them here we have is burgers disease this is a situation where we're going to have more decreased blood flow and that can cause the patient to have some pain discomfort and that's what we primarily see with / with our arterial peripheral vascular disease we're an odd phenomenon and disease is a situation where we get episodic vasospasm so the patient has some episodes where they have vasospasm occurring in the arteries and arterials primarily of the digits so it's primarily of the hand and this can be stimulated by a number of different things but you know one of the main things that that predisposes somebody tyranids phenomena is going to be a collagen vascular disease like scleroderma or smoking smoking can also predispose somebody to developing a peripheral vascular disease thromboembolism and i kind of mentioned this briefly before when we talked about the possibility of a DVT which is a deep vein thrombosis versus the other terminology which could be thromboembolism a venous thromboembolism so let's just talk about this and talk about thrombi and emboli for a moment so first of all we have a thrombus a thrombus is a clot that is forming in a vessel usually because we have some kind of damage to the inside lining the blood vessel so we have damage occurring to the blood vessel and a thrombus a blood clot is forming inside that blood vessel that is a thrombus a thrombus is not moving it's just a clot it's sitting there and embolism is a thrombus that's moving okay so an embolism is a blood clot that is moving through the blood stream and probably is going to get stuck somewhere eventually it's going to hit a small vessel and get stuck there a thromboembolism is a blood clot that has dislodged and is moving through the body so when we talk about an embolism we're talking about something that has mobilized through the blood stream a thromboembolism we're talking about a blood clot that is mobilized and so very much so a thromboembolism and an embolism are very much the same thing it's just thromboembolism is very specific to it being blood versus an embolism could be some other kind of matter in the body

Channel: David Woodruff

Views: 52,801

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Keywords: Nursing, Nursing Student, Cardiac Pathophysiology, Student nurse, Nursing education

Id: I9KUjGMKkH8

Length: 61min 45sec (3705 seconds)

Published: Thu Feb 07 2013