Cardiovascular Alternations (part 2)

coronary artery disease is a disorder where the patient has decreased blood flow going to the heart so this is a situation where we have maybe an athletic erotic disease that's going on or whatever and we're not getting enough blood flow to the heart so coronary artery disease starts as being athletic erotic disease and then it starts working into causing additional problems with our patient such as angina and myocardial infarction so this diagram here is just showing you the process that occurs with endothelial injury and then the resultant changes that occur in the vessel so you notice at the top we have a fairly normal looking vessel here maybe it's become damaged in some way and microscopically over on the right-hand side we're starting to get some response to injury that starts to cause this fatty streak the fatty streak is the result of having fat molecules that are kind of bunching together here with the underlying inflammation so the underlying inflammation is causing the patient to have things like platelets and fiber and etc start to connect there collect there and the fatty streak the fat molecules then start collecting on top of that on top of the fat molecules then we start to get this collagen or this fibrous cap and the fibrous cap is now going to contain the whole thing so that it can't easily be removed from the body unfortunately what also happens is the fibrous cap can tend to keep this thing well contained where it's not getting oxygen and then we start to develop a necrotic core and the necrotic core will then continue to maintain inflammation over a long period of time now this is a complicated lesion at the bottom where we also have a thrombus so we've got not only this fibrous plaque that's inside the patient's body but we also are inside the vessel but we also now have platelets that are sticking to it and we have a thrombus that has form and that thrombus can continue to get bigger and bigger and bigger and block the vessel or it could break free go downstream to a smaller vessel and block the smaller vessel risk factors for coronary artery disease we break those up into two major categories are non-modifiable risk factors not a whole lot you can do about your age or your gender your ethnicity your family history okay so not a lot you can do about that stuff so those are the non-modifiable risk factors but we want to know about them so we we were going to ask our patient about anybody else in their family who's had any kind of cardiac disease we're going to look at age we're going to look at gender and and I to get an idea as to whether or not this patient may be at high risk for developing coronary artery disease there are several modifiable risk factors though elevated serum lipids we can take medications to help decrease the amount of cholesterol that's in the body or you know obviously diet would be the great thing to do first is to modify the diet so we can decrease the amount of cholesterol in the system but if not then we can take medications for that that will help to lower the cholesterol those are called statins st atin statin hypertension is a modifiable risk factor in that we can lower the patient's blood pressure with medications tobacco use so we can have the patients stop smoking and using tobacco tobacco in general is going to have nicotine and nicotine is a stimulant and that stimulant is going to cause the patient to have an increase in heart rate and it also rotates because of the carbon monoxide and other chemicals inside the cigarette smoke itself it'll irritate the inside lining of the blood vessel to physical inactivity obesity diabetes metabolic syndrome is a combination of things that go into determining whether or not a patient is going to it's kind of a triad of different modifiable risk factors that the patient can have that will lead to the patient developing coronary artery disease psychologic states can also depression for example and homocysteine levels almost cysteine is one of those things that we can look at we can assess we can take levels of etc and find out what the patient's almost cysteine level is this is part of the inflammatory response so we can modify it by modifying information well the worst result the worst end result of having a patient have athletic disease would be myocardial infarction and in a myocardial infarction we have a deprivation of our blood supply now let's take a look first at what's happening with a temporary loss of blood flow to an area of the heart we get what's called reversible ischemia and typically in most cases we call that stable angina we can also have another condition it's called unstable angina where there may be some injury that's occurring to the patient's myocardium but it can be reversible in many cases atlas chromatic plaques can form in the coronary vasculature and they can be stable plaques or unstable plaques a stable plaque is simply just decreasing the amount of blood flow that's going through that vessel an unstable plaque on the other hand this could be really dangerous because it could break free it can go downstream it can cause a clot and totally occluded vessel which could cause the patient to have a coronary syndrome and by the way we call these things now acute coronary syndromes and the reason why we use that terminology is that terminology will then encompass everything from angina to myocardial infarction so it encompasses more things than just breaking it down and saying okay the patient's here because they have Anjan to the patients here because they have myocardial infarction instead we're just going to say hey the patient's got acute coronary syndrome which encompasses all of those things myocardial infarction in this situation the patient's got sustained ischemia for greater than 20 minutes we call that a myocardial infarction because we're going to have damage to the myocardium in fact we're going to happen to chronic damage to the myocardium we're going to have some anaerobic metabolism occurring in the myocardium itself which could help to maintain the metabolism help to maintain that that musculature for a period of time and we can break down our Mis into two different kinds we can call them a ST segment elevation MI or a non ST segment elevation mi what this refers to is it refers to whether or not we have changes occurring on our EKGs so we would take an electrocardiogram of the patient to try to determine whether or not they have a myocardial infarction if in fact there were changes on that EKG we would call it a STEMI ST segment elevation mi if there were no changes and we had to find out that the patient had an MI as a result of looking at our enzymes or cardiac enzymes we would call that a non-st segment elevation Am I so let's break this down again here a little bit here's a little bit more information about the two of those when we talk about am I being a nun ST segment elevation mi so non-stemi all right those are mi is that in general because it's not causing EKG changes in general it's going to be a smaller mi then would be what we call a STEMI ST segment elevation mi so we're getting EKG changes and we also refer to that as being transmural transmural means it's going all the way through the muscle so sub n de cardio means is not going all the way through the muscle is just going into the epicardium and Accardi I'm sorry and it's not going all the way through so that's a little bit different however rather than talking about them in terms of transmural versus sub into cardio we refer to them by whether or not they have EKG changes so in other words we say it's a STEMI or it's a an STEMI now to get an idea as to what's going on with our patient here and how this all fits together take a look at the diagram here and the underlying variable that's happening in this diagram is athletic erotic disease so the underlying thing is athletic disease and what we have is a continuum and we're flowing down through the continuum based upon how long the amount of damage has occurred to the heart so over on the left hand side we just get a little bit of a disruption of blood flow to the patient's heart and we develop ischemia that's reversible that's called stable angina so stable angina we have ischemia to the myocardium but it's totally reversible it goes away as soon as the patient sits down rests or takes a nitroglycerin tablet something that's going to allow those coronary vessels then to fill again like they normally should next we move into an area where we start to get injury occurring to the myocardium now this injury could recover if we're giving the myocardium enough time to be able to recover etcetera we could recover so it's possible that that could recover this is called unstable angina and unstable angina see we're kind of in the middle here it could go either way we could go a kind of this stable area and just have a ski Mia or we continue to progress into necrosis which would be a really bad situation because now we're getting into that myocardial infarction when we're getting a myocardial infarction whether it's an honesty segment elevation mi okay that's the one without EKG changes or an ST segment elevation mi that's the one with EKG changes either way we're getting necrosis of the myocardium now remember again necrotic tissue is dead tissue okay so it's not going to function it's not going to contract it's not going to carry electrical energy so we have basically a dead area of the heart and if that dead area the heart is very large then the cardiac output is going to be dramatically affected disorders the heart wall in addition to myocardial infarction can include things like a pericarditis so we can have problems with the pericardium itself or we can have a pericardial effusion where we have fluid leaking into that space between the pericardium and the myocardium we can also have disorders of the myocardium itself like cardiomyopathies and we can have disorders of the endocardium that's the inside lining of the heart which can lead to valvular disorders such as stenosis or regurgitation let's take a look at some of those disorders first of all disorders of the pericardium the pericardium remember again is the outermost layer of the heart and the pericardium is keeping the heart in place so it's holding the heart in place but we can develop in some cases maybe from infection or trauma etc we can develop an inflammation of that layer one of the main things that happens with this inflammation first of all it's going to be painful but the next thing that happens with this inflammation of the pericardium is that it can develop fluid you know when you get inflammation in parts of the body let's say that you sprain your ankle and your ankle swells okay you're getting fluid in that area as a result of inflammation well if we get fluid in the pericardium as a result of inflammation that's going to start to build up fluid in there and squeeze the heart and that's going to cause what's called a tamponade this is a picture here showing a patient who had pericarditis now you look at the outside lining of the heart that should be nice and smooth and glistening instead it's all rough so we obviously had a lot of inflammation on the outside lining of the heart and that can cause some significant pain and if it's infectious that could really be a problem for our patient as the infection starts to cause dysfunction of the myocardium - pericardium well what can happen as a result of having maybe a pericardial effusion or pericarditis is the patient can end up developing fluid in that pericardial cavity we call that a pericardial effusion well in many cases that may reabsorb on its own or we may have to send the patient down to the o.r and drain that fluid off if the fluid creates too much if it gives with too much fluid in that pericardial sac we can develop what's called a pericardial tamponade in which case the fluid has starting to build up and it's starting to compress the myocardium and compressing the ventricle and so there's not enough room to be able to fill the ventricle constrictive pericarditis this is a situation here where we're going to start to get some scarring and calcification etc in the pericardium in the pericardial sac and it's going to decrease our cardiac output because the heart can't fully fill I can't swell out enough and let enough blood fill into the myocardium cardiomyopathy is a term that's used to describe a change in the size and/or the shape of the myocardial cells now this is a heart here and a patient who had what's called dilated cardiomyopathy dilated cardiomyopathy can happen in patients who have heart fire for example and the heart just in it's a attempt to try to pump better what ends up happening is that the muscle starts changing its size and shape and now you can see here this doesn't look anything like a heart anymore it's this big round thing instead of having that nice v like shape that our heart should have this is this big rounded thing now that's not going to contract very well and we're not going to get a good cardiac output as a result of it so the problem with cardiomyopathy is we get a change in the size and the shape of the and that leads to decreased cardiac output we can have other types of cardiomyopathy including hypertrophic this is the thing that we used to call a ventricular hypertrophy so the muscle is starting to build up and get bigger and that's impeding our ability of the heart to be able to constrict to contract restrictive on the other hand is a situation where we're also going to have problems with being able to have a normal cardiac output let's take a look at these pictures here I think this might make it a little bit more obvious to you as to what's going on here's a normal heart at the top so it's showing you the left atrium and the left ventricle and you notice the shape of the left ventricle that we see there a nice V like shape go over to the right side and you see we have dilated cardiomyopathy that big round heart like we saw in the picture okay now that's not going to pump very well remember the ventricle is going to contract as a whole like one big muscle and try to pump the blood out well it needs to have a V shape to do that if it's got this rounded shape to do that then there's going to be a lot of blood it sits in the ventricle that doesn't get pumped out on the other hand we can have letters see at the bottom there hypertrophic type of cardiomyopathy where the patient has hypertrophy of the ventricular muscle and now you can see the ventricle is so small we can't fill it adequately in order to maintain an adequate cardiac output on the other hand we can move over to D over here where we have a restricted and then restrictive cardiomyopathy the ventricle does not contract very well because of fibrous type disease the endocardium is the inner lining of the heart and remember again that the valves attached to the inner lining of the heart so one of the main problems we're going to have with disorders of the endocardium such as endocarditis is that it can damage our heart valves and it can lead to either stenosis or regurgitation of our valves so let's take a look at value ler dysfunction here for a moment when we're talking about stenosis and regurgitation of the valves what we're talking about is a dysfunction in a way that the valves are normally working stenosis means they're narrowing so the valve is narrowing okay well let's say we've got a hundred people that we need to try to get out of a room and we have two doors but only one of the doors works well that's kind of like a narrowing of the valves we're not going to get people out of that room as fast as if we had the two doors open so that's the same kind of thing that's happening in the heart with the valves is that if the valve is not opening fully then we're going to have trouble moving fluid past it's a forward flow is going to start to decrease and that increases the workload on the heart that's from stenosis and narrowing of the valve the other possibility is a valvular regurgitation in this case here the valve isn't narrowed it opens up like it's supposed to blood is able to pump through the valve okay so no big deal there but it doesn't shut all the way and because it doesn't shut all the way what's going to happen then is fluid moves backward so we're going to get the backward flow of fluid as a result this is a picture here showing a valve that has become diseased and you can see all of the junk on that valve that valve should have a nice rounded smooth shape to the the edges as they're coming together and it does not they're kind of all chewed up and that's going to lead to dysfunction there's going to be leakage of fluid through that valve where there Mele should not be there's some great videos here about valvular disorders so make sure that you're using these links and getting out there and taking a look at these different valvular disorders these are included on your PowerPoint or you can cut and paste them from your screen but probably easier just to get them right off of your powerpoint that's available on your course shell mitral stenosis is a situation where the mitral valve okay now when we're ever talking about valvular disorders first of all in your mind think where is that valve and then what is the situation that's wrong with it so in this case here where is the valve mitral valve is between the left atrium and left ventricle all right what is the problem with the valve stenosis that means it's narrower than it's supposed to be so if stenosis decreases forward flow that means that flow is not going to get to the ventricle and we're going to have a decrease in cardiac output so this talks about some of the different Scituate that can lead to a patient developing mitral stenosis such as rheumatic heart disease a or text enosis okay again whenever you're talking about different valves think about the valve and think about the problem okay the aortic stenosis the Artic valve is the valve that's coming from the left ventricle to the aorta it's stenotic so it's narrowed that means we're not going to be able to pump out as much blood from the ventricle moving forward into the aorta and our cardiac output will decrease acute rheumatic fever this is a diffused inflammatory process that's occurring in our patient that can cause the patient to develop rheumatic heart disease and then the big problem with that is the patient's going to develop at least possibly develop a valvular dysfunction infective endocarditis now we have an in situation here where we have a bacteria that has gotten into the patient's body it's infecting that inside lining of the heart and again one of the main things we have to be concerned with here is the possibility that that's going to start to damage the valves sure it could damage the inside of the heart and that causes problems too because we're going to start to roughen up the lining inside the myocardium and that can cause platelets to stick there can cause things to stick there and it can cause emboli to start to form so there's all sorts of problems that can result as a result of endocarditis but one of the main things we're concerned about is that damage the length of the valves and having long term valvular dysfunction some of the manifestations we see of heart disease include the thing called dysrhythmias dysrhythmia is an abnormal heart rhythm so it dysrhythmias an abnormal heart rhythm the patient may have missed beats they may have additional beats they may have a rate that's too fast or too slow these are all abnormal rhythms to the heart we should have a nice steady feeding of the heart that is consistent that would be a normal rhythm and when we have anything that's not normal we call it a disc rhythm eeeh another term you may hear is arrhythmia these terms in clinical practice are used interchangeably really arrhythmia means that there's no rhythm so just arrhythmia means there is an abnormal rhythm so really the I guess at least grammatically the better term would be dysrhythmias but you may hear both of them used in clinical practice now what we're seeing here at the bottom of the page is an EKG that came from a patient even if you don't know what that means you don't know how to read it one thing you could say as well it looks like that thing is pretty fast so that would be a dysrhythmia because the rate is too fast in fact the rate in this patient is very fast and the rhythm here that we're seeing is called a ventricular tachycardia ventricular tachycardia is an abnormal rhythm that can lead to cardiac arrest this diagram here is showing some of the things that can happen when your patient has myocardial disease so let's take a look at some of these different things and what's how they're affecting each other left ventricular dysfunction starting at the bottom of the page can cause electrical instability in our heart so if the ventricle isn't functioning very well it can cause electrical instability the electrical instability itself thing can cause more left ventricular dysfunction the electrical instability can cause a scheme eeeh because we're not getting a normal rhythm in the heart at the same time the ischemia can cause left ventricular dysfunction whereas left ventricular dysfunction and cause a scheme you see how we can get into this vicious cycle where we're just moving around this thing here and the patient's cardiac function just keeps getting worse and worse and worse yes that can happen as a result of this process so something to keep in mind here is that this can happen as a result of this process take a look at some of those components as it goes along the diagram you might might want to pause the video here for a few moments to look at the diagram and really take in everything that's telling you when a patient has decreased cardiac output there are going to be compensatory mechanisms that kick in in the body and those compensatory mechanisms are the sympathetic nervous system the renin-angiotensin system we also called that before the renin-angiotensin aldosterone system and aldosterone itself okay so those three things are three major compensatory mechanisms that kick in when the patient has a decreased cardiac output these compensatory mechanisms have no idea the body has no clue as to what's causing the decrease in cardiac output the decrease in cardiac output could be caused by any number of things it could be caused by dehydration could be caused by a cardiac problem which is what we're talking about now could be caused by sepsis we don't know the body doesn't know when the body doesn't care the body will respond in the same way every single time and it stimulates these compensatory mechanisms all right let's take a look at this in terms of a patient who is dehydrated with a patient who's dehydrated this stuff makes sense so you're going to walk across the desert not bring a canteen with you your body is going to try to maintain cardiac output for as long as possible it does that by stimulating the sympathetic nervous system and the sympathetic nervous system is going to increase your heart rate and your cardiac output maintain your cardiac output for as long as possible next the remin intention system kicks in and is going to increase your blood pressure to again maintain cardiac output lastly aldosterone kicks in and aldosterone is going to tell the kidneys to hang on to more fluid again to maintain cardiac output these things work when you're dehydrated what about in a situation though where a patient has a cardiac problem in a cardiac problem and in patients let's say having a heart attack they have decreased cardiac output because our heart isn't functioning very well sympathetic nervous system kicks in and tells the heart to beat harder and faster don't you think it would have if it could have okay that's not going to help the renin-angiotensin system kicks in and it causes vasoconstriction it kinks the tubing well that's not going to help think about your guard nose we're going to decrease our cardiac out but we're taking the tubing the an astronaut storm system kicks in it tells the kidneys to hang out a more fluid we don't need more fluid we can't even pump the fluid we have so these compensatory mechanisms are all going to be dysfunctional and a patient who has a cardiac problem so what do we do about them we're going to treat the sympathetic nervous system by giving the patient beta blockers that's of medications going to block the sympathetic nervous system we're going to treat the renin-angiotensin system by giving the patient ACE inhibitors some people can't tolerate those so instead we'll use a arby's angiotensin receptor blockers we're going to block the aldosterone system by using aldosterone antagonists okay don't worry so much about the medications at this point in time but just understand that we have mechanisms we can use we have medications we can use to block these compensatory mechanisms and the reason why we want to do that in our cardiac patient is because their compensation makes them worse left heart failure and heart failure in general is the result of our compensatory mechanisms making the cardiac function worse in that particular patient so we get symptoms of pulmonary vascular congestion inadequate profusion of our systemic circulation as fluid is backing up from the left side into the lungs and not getting out there into the tissue now we can break up heart failure into two different types we can caught systolic or diastolic with this picture here is illustrating what happens with our cardiac output in patients who have systolic and diastolic dysfunction now these diagrams are illustrating the ejection fraction of the heart the ejection fraction is the amount of blood that is pumped out of the heart with each contraction so with a normal contraction of the heart we pump out about 65 to 70 percent of the blood that's in the heart not every drop but we pump out about 65 to 70 percent with a patient who has systolic dysfunction systolic is contraction so the patient has an inadequate contraction of the heart well they're going to have a low amount of blood volume pumped out of the heart in fact now this patients only pumping out 35 percent of the blood they have an art that's systolic dysfunction and obviously if we're only pumping 35 percent forward that means that we are not getting a lot of cardiac output and blood is going to start to back up and he and diastolic dysfunction is the result of inadequate relaxation of the heart so the heart's not fully relaxing so it can't fully fill now the heart still has a strong contraction so we're able to pump out 65% of what's there but the way the patient develops heart failure in this case is because we started with less look at the volumes in those three compartments we started with less so even though we're pumping 65% we started with less to begin with and we still end up having a decreased cardiac output right-sided heart failure most commonly is going to be the result of left-sided heart failure so it's as commonly caused by hypoxic pulmonary disease yeah if we have isolated right-sided failure it would be commonly from hypoxic pulmonary disease could also be from pulmonary hypertension but most right-sided heart fire is the result of left-sided failure the left side fails backs up to the lungs and backs up into the right side and then the right side fails to shock is a situation where we have decreased perfusion of the tissues so in shock we have decreased perfusion of the tissues now there's a lot of things that we use to help us to be able to determine shock in other words oftentimes we will look at things like our vital signs etc to tell us that the patient has shock but shock state itself is a state of decreased perfusion to the to the tissues and that is not dependent upon the blood pressure or the heart rate so much as it is what that particular patient needs shock can be divided up into different types including hypovolemic cardiogenic neurogenic anaphylactic and or septic depending upon what it is that's causing the patient to have shock so these are all different ideologies for shock but shock itself is going to be the same process irregardless of what it is that starts it in the shock again is decreased tissue perfusion it's decreased perfusion of the tissues and that's going to be the same process whether it's hypovolemic cardiogenic etc untreated it's going to overwhelm the compensatory mechanisms and the patient's going to have cell death and can progress to multi organ dysfunction syndrome in which case now we're going to get secondary damage to organs that are even distant to the original problem so let's say the patient has cardiogenic shock which comes from having a heart attack or having decreased cardiac function so the patients get decreased cardiac function that's causing the patient to have shock so the heart's not pumping well cardiac output goes down the patient develops shock and it's caused by cardiogenic it's caused by the heart if that does not get treated then the decreased cardiac output over a long period of time will cause other organs to fail like the brain like the kidneys because they're not being perfused this is the thing that happens it's called multi organ dysfunction syndrome all right now this is kind of a busy little slide here so let's take a look at it and dissect it a little bit but what is showing is what happens with impaired cellular metabolism that's caused by decreased tissue perfusion so a lot of stuff going on here you don't need to know all this detail when we're dealing with talking about our cardiovascular system but this is a slide just to look at for a while and try to follow through and see what parts of this you you've got already and what parts of this still are kind of a little bit troubling to you so as we look go over let's go over to the right hand side here which says impaired glucose use and you remember you learned about earlier in the end of course you learned about decrease glucose use in a patient who has anaerobic metabolism and that leads to an increase in pyruvate which then leads to the patient developing an increase in lactate and metabolic acidosis so you can kind of see how some of those things are starting to fit in here a little bit over on the left-hand side impaired oxygen use leads to anaerobic metabolism again there's your lactate and decrease ATP production dysfunction of the sodium potassium pump increases in intracellular sodium and water remember if the pump isn't working we can't keep that sodium out and sodium starts rushing in water follows it now we have cellular edema which then can cause destruction of the cell so follow this thing through some of these different pathways here and see if you can explain it based on some of the things that you've already learned as to why these processes are occurring in a patient who has decreased tissue perfusion hypovolemic shock is a type of shock that's caused by a lack of volume so the problem here is a lack of volume we've lost volume somewhere the problem with hypovolemic shock is you can't put it back okay so if the if the patient was bleeding you can't just grab up all the blood and put it back in okay so whatever the patient loses we're going to have a hard time replacing it now you're going to hear in the clinical area you're going to hear people talk about giving replacement fluids okay replacement fluids don't replace what was lost I can give this patient blood from the blood bank but that's not his blood see that's going to be a little bit different and it could cause some kind of reaction in the patient's body what if he's got burns and he loses a lot of fluid from burns I'm not replacing the fluid that's been lost when I give IV fluids I'm giving that patient a cheap substitute so whatever we're going to do to quote replace fluids is going to be a cheap substitute therefore the number one thing we want to do in hypovolemic shock is to stop the loss plug the hole let's stop this loss from continuing but the problem that occurs here is that the patient has decreased volume so there's not enough volume to pump and then the patient ends up developing hypovolemic shock so let's follow this diagram down at the top we have decreased intravascular volume causing decreased cardiac output again the heart is just a pump it's going to pump what it gets and if it doesn't get anything to pump it doesn't have anything to pump into cardiac book goes down okay pretty simple that if there's no volume coming in there can be no volume coming out on the right-hand side of the screen we have decreased cardiac output which is going to cause our catecholamine release remember we have those compensatory mechanisms the first of which is sympathetic nervous system there's our sympathetic nervous system it's going to cause an increase in heart rate and contractility which will temporarily increase our cardiac output on the other side we have our in our interstitial fluid we have our aldosterone secretion so those things are going to help to hold on to volume so increase in heart rate increase in volume our cardiac output is at least temporarily increased more volume loss okay now we're overcoming what those compensatory mechanisms can do and our cardiac output further decreases and our tissue perfusion decreases and then we get impaired cellular metabolism at the tissue level cardiogenic shock is caused by a pump failure in other words the heart has failed so cardiogenic cardiac is referring to the heart most commonly this is going to be the result of the patient having a myocardial infarction myocardial infarction causes cardiogenic shock more frequently than other things because it's sudden and we have now an area of the heart that's no longer functioning and the heart doesn't get a chance to accommodate for that some of the other things that can occur here like valvular dysfunction and heart failure the patient may be able to accommodate that for that and not develop shock as a result okay let's take a look at this picture our cardiac output has decreased because the patient has a myocardial infarction heart failure etc that causes those compensatory mechanisms to kick in to try to maintain our preload our stroke volume okay remember preload is the volume of fluid coming to the heart okay and well we already have a lot of volume coming to the heart we don't need more but the body is telling you to hang on to more that's going to increase our myocardial oxygen requirements cardiac output injection fraction are going to temporarily at least increase when we have these compensatory mechanisms but eventually they're going to decrease as a result of further ischemia and for the pieces in tissue perfusion neurogenic shock is caused by massive vasodilation so we have unbalanced parasympathetic activity remember sympathetic activity causes the fight-or-flight it causes the increase in our heart rate increase in our blood pressure okay so the sympathetic system is causing vasoconstriction maintaining the pressure in the vessels parasympathetic is just the opposite parasympathetic is causing vasodilation relaxation of those vessels if those vessels relax we won't have enough pressure in there to maintain blood pressure and that's what causes neurogenic shock neurogenic shock is going to be caused by having either a some kind of a lesion in the spinal cord that that's going to interrupt our sympathetic nervous system innervation or a central nervous system problem a problem that's occurring in the brain so we have a decrease in our sympathetic stimulation with an increase in our parasympathetic usually that's because the sympathetic stimulation has been cut off so we've had an injury in that spinal cord and we no longer have the sympathetic system innervating the body so we get a decrease in vascular tone vasodilators Collor resistance goes down which causes then a decrease in cardiac output and a decrease in tissue perfusion anaphylactic shock is the result of having a widespread hypersensitivity in other words allergic reaction as a result of this allergic reaction the patient gets a massive vasodilation so this is very similar in what happens physiologically in neurogenic shock it's just the cause is different in this case the cause is the inflammatory response remember inflammation causes vasodilation so here we have a massive inflammation that's occurring as a result of an allergy and that massive vasodilation then causes the patient to drop their blood pressure and decrease their tissue perfusion so here we have the allergen the allergen and this top part here is just showing you the process of developing an allergic action so we develop an antibody IgE and a complement histamine etc is going to stimulate the inflammatory response which increases capillary permeability and causes vasodilation those things are going to lead to a relative hypoxemia eye relative hypovolemia I'm sorry so this he'll ative hypovolemia the fluids out there it's just out there in the tissues it out there and in the peripheral system so what we need to do in order to fix this is we're going to have to get that fluid back into the central circulation by giving the patient something to vasoconstrict them but in the meantime we have decreased cardiac output which is causing impaired cellular metabolism so here are some causes of anaphylaxis the treatments listed over on the left hand side they're epinephrine and benadryl those things are directly affecting the allergic reaction steroids are going to decrease inflammation okay paps it is an h2 blocker that's a histamine to blocker which can blocks some of the histamine that is not blocked by the benadryl septic shock in septic shock we have a situation where the patient develops an infection and that gets into the bloodstream now this terminology can get a little bit confusing so I'm sorry about this we're going to get into a little bit more definitions here in just a moment but when we talk about septic shock most the time what people are thinking of as they're thinking of an infectious process that's occurring in the patient's body and because of infection we get an overwhelming out-of-control inflammatory response and remember again what happens with inflammation we get vasodilation so this diagram here is just showing how we get this inflammatory response started we have the gram negative gram positive organisms that gets into the bloodstream and then that is stimulating our inflammatory response if you go down to about halfway down the page it talks about Sears s IR s that's the systemic inflammatory response syndrome where we have this overwhelming out-of-control inflammation that's going on body and that causes the next step which is vasodilation hypotension and tissue inflammation tissue hypoperfusion eventually that leads to worsening of our hypoperfusion and multi organ dysfunction the pathophysiology of sepsis we talked about sepsis being both of the presence of a systemic infection and our systemic inflammatory response syndrome and then this causes the ultimate results we're going to see we're going to we're going to look at this in more detail here in just a moment some of the components of the systemic inflammatory response syndrome include white blood cells being released blown pro-inflammatory cytokine flam Ettore cytokines and tumor necrosis factor in interleukins okay let's take a look at this diagram a minute and see how all these things plug in together we have an initiating factor that's causing this thing and notice that the terminology is different the terminology says sepsis syndrome as opposed to septic shock this idea of sepsis we have found out is that not only is it bacterial and an infection that causes this whole process to occur but it can also be injury or ischemia because of that they're now changing the terminology somewhat to be sepsis syndrome so if you hear that a patient is septic I think in most cases what you're going to find is the patient probably has an infection however sepsis syndrome could include the same results as septic shock from an infection so let's take a look at what happened we're going to follow infection across and then plug in one of these other ones so the patient has an infection patient comes to the hospital because they have a urinary tract infection bacteria from that urinary tract infection get into the bloodstream and they cause an overwhelming out-of-control inflammatory response that's this thing here in the middle the inflammation part and we also call that Sears systemic inflammatory response syndrome Sears so that's this overwhelming inflammation that's happening in the middle one of the main components of inflammation is we get vasodilation that causes severe sepsis in severe sepsis we have massive vasodilation going on that's causing a drop in the patient's blood pressure that drop in blood pressure will respond to giving the patient IV fluids if the drop in blood pressure does not respond to IV fluids and continues to get worse we call that septic shock lastly if this process continues to go on for a long enough period of time will start getting secondary organ dysfunction as a result of the other two components involved in inflammation which are capillary permeability and clotting capillary permeability causes edema clotting causes little micro clots inside the tissue and those two things together are going to cause tissue damage in the lung they're going to cause a RDS in the kidney they're going to cause acute renal failure and the hematologic system we're going to use up our platelets in the patient will develop a process called di C disseminated intravascular coagulopathy next we can get liver congestion liver failure heart failure and then anoxic brain injury these results a multi organ dysfunction are the direct result of the systemic inflammatory response that you see in the middle of the screen which were initiated by that infection injury or ischemia so multi organ dysfunction syndrome what happens here is that the patient is having damage to two or more organ systems as a result of this initiating factor and the systemic inflammatory response failure of two or more of the organ systems is going to cause a very high mortality rate in our patient so even though the patient was a fairly healthy patient to begin with once we have two or more systems starting to fail the mortality rate increases dramatically multi organ dysfunction syndrome is really just a name for the fact that we're getting distal injury to organ systems outside of the original organ that was damaged from the shock so maybe it's a myocardial infarction that's causing the patient to have decreased perfusion and the systemic inflammatory response syndrome that is activated and then other organ systems distal to that become involved primary multi organ dysfunction syndrome occurs with the direct injury from whatever the underlying problem is then secondary and this is what we usually refer to as being most of our mods is the consequences of our systemic inflammation signs of organ dysfunction include respiratory failure again that would be a indication of a RDS acute renal failure hematologic dysfunction we'd see that evidenced by seeing a decrease in your patients platelet count liver failure we can see that evidenced by an elevation in our liver enzymes cardiac dysfunction and then finally anoxic brain injury we're going to see that evidenced on the EEG and maybe something like an MRI of the brain risk factors include age the older the patient is and we should also add to that the very young the very old and the very young have less control over their immune system then do adult patients baseline organ function is a risk factor if your patient already had some underlying renal dysfunction and then has multi organ dysfunction on top of it much higher chance that they're going to end up having dysfunction of the kidneys I mean a suppression malnutrition inadequate or delayed resuscitation can also have an effect on how much multi organ dysfunction occurs significant tissue injuries the most common cause of all multi organ dysfunction syndrome mods is septic shock so overall some of the symptoms we're going to see as a result of shock are highlighted on this page here early signs in blood pressure could be normal early sign and our heart rate could be a little elevation skin color may still be normal skin may be a little cool and moist the patient may be a little anxious and the respiratory rate may be a little increased at this point in time in the early phase remember our compensatory mechanisms are kicking in in early shock later in shock if it's allowed to persist and the patient's blood pressure start to fall we're going to see other symptoms the blood pressure now is following the heart rates up and the heart rate is now becoming weak because we don't have enough blood pressure to maintain a nice solid bounding pulse normal our skin color becomes pale and the skin becomes cool maybe moist at this point or maybe even dry the patient's going to start to lose consciousness and respirations start to become more shallow as a patient doesn't have enough energy getting to a respiratory system to continue to have good respiratory function well I hope you have enjoyed our presentation of alterations and cardiovascular function and that this helps you in forming your study and figuring out what parts of the cardiovascular system are most important to study when you're looking at your cardiovascular dysfunction thanks for joining me until next time bye now you

Channel: David Woodruff

Views: 16,330

Rating: 4.9444447 out of 5

Keywords: Nursing, Nursing education, nursing school, student nurse, pathophysiology

Id: Q0voWXPCsm0

Length: 47min 33sec (2853 seconds)

Published: Fri Feb 08 2013