![[title]](https://draxe.com/wp-content/uploads/2016/05/Frozen-Shoulder-Graphic.jpg "[title]")
alright. let s talk myocardial infarction.when we talk myocardial infarction, we re of course talking about a heart attack. now,this is an important disorder to understand because it affects a lot of americans andit s something that you re going to see in your work in the hospital either directly,as patients have heart attacks, or you ll have patients with history of heart attackor stents, etc, that you ll have to understand how to take care of them and how to best providea appropriate therapeutic nursing care for these patients. okay. so, very briefly, let s talk about exactlywhat heart attack is. so, what happens in heart attack is, blood flow stops to partof the heart causing damage or death to the
heart muscle. okay, so that s really all heartattack is. what happens here, you can see, they ve taken this vessel here and they veblown it up. so, what happens is, you have this plaque build up and blood clot, and whatthat does is it impedes blood flow pass this point. so, of course, once blood can t getdown to this distal portion of the artery, we re not allowing oxygen to get to the muscles.okay, so when oxygen is unable to get to the muscle, this muscle dies. if that muscle dies,of course, we re looking here like a ventricle here, if that ventricle dies, that muscledies, it s not able to squeeze, we re not getting cardiac output, we going to have a,this will lead to, depending on the size of the damage, either heart failure or death,as the heart muscle is no longer able to do
it s job. okay, so it s an emergent disorder,something that has to be treated very quickly, and we have to clean up this clot and allowthat blood to flow and restore oxygen supply to that cardiac muscle. okay, so when we talkabout heart failure or myocardial infarction, i really want you to think of it as a vessel,i want you to think of it as a vascular, let s do that, i want you to think of it as avascular disorder, okay. because, what it really is, is we have poor vessels, and becauseof that, we re going to lose our blood flow. so, things that are going to lead to m.i.are the things that are going to affect our vessels are gonna be vascular type disorders,okay. so, really quickly, let s just draw our heart and let s talk about a couple ofthe main arteries really quick. so, in here
we have our aorta coming out. so, coming offthe aorta here, we have our right coronary artery, this kinda come down this way, andthen we have our left main coronary artery coming kind of this way, and then off of that,we have our circumflex coronary artery, okay, so that s kinda supply the back end here.and then, coming off of that left main coronary artery, we re gonna have our left anteriordescending coronary artery. okay, so, left main, left main coronary artery, right coronaryartery, left anterior descending coronary artery, and then circumflex coronary artery.okay, so those are the main ones. okay. so, what happens when we have a major heart attack,is one of these main vessels is going to become occluded to the point of no blood flow distilledto the occlusion. so, right coronary artery,
left main coronary artery, left anterior frontof the heart descending coronary artery, and then we have our circumflex coronary artery,okay? so, those are the main vessels and those are the ones we kinda keep in mind becausewe can actually tell based on ekg where the heart attack is. you know. so, let s, before i get ahead of myself, lets dig in where we need to dig into. so, as i said, it s really a, it s a very commondisorder, 735,000 americans have heart attack every year based on the information from thecdc. now, some of the big risks factors are gonna be high blood pressure, high ldl, smoking,and these are key risk factors of heart disease. and the problem is about half of the americanshave at least 3 of these risk factors. so,
half of americans either have blood pressure,high ldl, or are smokers. these are the 3 main leading causes of heart disease and heartattack. now, you can see, it s very regionally distributed here, kind of in our south wherethere s more, traditionally more fried foods, more sanitary lifestyles, less active, moresmoking. these are areas that are going to be have higher incidents of heart diseaseand heart attack. now, 1 in every 4 deaths in america, nationwide, is due to heart disease.so, 25% of every single death is based on heart disease. okay, so again, it s somethingthat we really need to understand. now, like i said, we re gonna talk about m.i.as a vascular disorder, okay? so, let s talk about, knowing that, let s talk about whywe re gonna talk about as a vascular. so once
we talk about vascular disorder, we re goingto understand how it happens, some of the signs and symptoms we re gonna have, someof the causes and then the therapeutic interventions that we re gonna be able to do. so, modifiablerisk factors, like we said, smoking, we talked about hypertension. okay, so, smoking of courseis gonna lead to atherosclerosis and thereby lead to vessel damage. obesity, as well, youre gonna have higher lipids and that s going to lead to increased vessel damage as well.stress, more catecholamines in the system, more cortisol, that s gonna lead to vascularissues and possibly lead to m. i. hypercholesterolemia, like we said, high ldl, high low density lipoproteinsis going to lead to that occlusion, right? cause we get that high ldl, we re gonna buildplaque in our vessels, impede blood flow,
and that s gonna be the the cause for an m.i.diabetes. now, diabetes can obviously lead to vascular damage, okay. as we have thatvascular damage, those vessels become weak, we may have increased blood sugars more oftenand that s gonna lead to vascular damage as well. hypertension, of course, as well atherosclerosis,hardening of the walls, and more pressure trying to go to the system at any one point.and that too, is going to lead to vessel damage and possible m.i. and death as well. okay.so, again, vascular disorder and these are common things that are gonna lead to vasculardamage, okay? now, there s a couple of different types ofm.i. okay, and when we talk about m.i., again, we re talking about myocardial infarction,and there s some ways that we can see that.
one of the best ways to notice an m.i. isgonna be on an ekg. now, we re gonna be able to see on ekg the st elevation, okay, so were talking about st elevation myocardial infarction. you may have heard this term stemi before,that stemi refers to st elevation myocardial infarction. now, there s another type of myocardialinfarction and that s a non-st elevation m.i. or nstemi. okay, so on an nstemi, you re notgonna see these ekg changes, okay, specifically the st elevation. however on a stemi, youre gonna notice these ekg changes. and the reason for that is, because, what happensto cause this st elevation is that you have complete occlusion, complete occlusion ofa major coronary vessel. now, once we have that complete occlusion of one of these majorvessels that we talked about a minute ago,
we re leading, it becomes incredibly an emergentsituation, okay? so, what we have here is we have our ekg right? we have our p, q, r,s and t. okay, so this would be a normal ekg of someone, just normal all about, and thenwhat happens is, as they develop this complete occlusion of this major vessel, is this s-tsegment is going to begin to rise, and then it kinda becomes one big wave as it progresses.so, here we have our s and our t are both elevated. so, rather than this seeing anyof this electrophysiological change here, we re gonna see this s and t kinda just becomesone big wave and that s the st elevation. okay. so, that s kinda the ekg change thatyou re gonna notice on this page. and so, depending on where the actual infarction is,is gonna depend on what lead you re gonna
see this in. okay, so, whether it is inferior,posterior, heart attack, depending on where the heart attack is, it was gonna tell youwhat lead you re gonna actually see the change in on your 12-lead ekg. now, we don t talka lot about 12 lead here because it s not necessary for nclex. but once you understand12-lead and kinda understand these ekg changes, you re gonna see, you ll be able to look at12-lead ekg and you ll be able to know exactly what coronary artery is affected by this,because, the st elevation is going to show up in the lead that corresponds to the arterythat is affected. okay. so, some of the other things that were gonna do with a patient who is suspected to have an m.i., is we re going to draw whatis called cardiac injury profile, or cip s,
as what we call them. so, if a patient thatcame in with an abnormal ekg, coming with chest pain, we re gonna run our cip s. okay.cardiac injury profile. so, if you wanna sound really smart, and clinical or something, saywe ll do any cip s on this patient. okay, and so, those are kind of 3 major labs thatwe re gonna draw. troponin, ck-mb and myoglobin. now, let s talk a little bit about these individually.so, troponin, we re specifically gonna draw troponin i and troponin t. the one you regonna see most often, looked at and referred to is gonna be your troponin i, okay? thesetroponin i and troponin t are found specifically in cardiac muscle, and they re release whenthere are cardiac muscle damage, so because of that, it s the most sensitive to cardiacdamage. so, that s one of the questions that
you may see on nclex is which laboratory valueis most sensitive to myocardial infarction or cardiac damage. and, that s gonna be yourtroponin, specifically, like i said, you re gonna refer to probably most often to troponini. now, the level of your troponin is gonna peak at 12 hours. so, what you ll see is whensomeone has a heart attack, that troponin will rise, rise, rise, after about 12 hours,it s going to get to its peak level and then it will begin to lower down again and it maystay somewhat elevated though. so, again, troponin i and troponin t are the laboratoryvalues that you re going to be looking at most specifically with myocardial infarction.another one that you re going to look at is ck-mb. cratinine kinase mb. now, there are2 different kinds of creatinine kinase, you
re gonna have creatinine kinase mb, bb, butspecifically for heart damage, you re gonna look at mb. and that might be a question aswell. which of these laboratory values is checked, you know, with myocardial infarction,or something like that. there maybe ck-mb, ck-bb, and your correct answer there is gonnabe ck-mb. now, it s found almost, the mb form of ck is found most, almost entirely in heartmuscles, it s release with heart damage as well, its peak time is a little bit longerthough. so, in order to get a more appropriate value, something more specific, we re gonnawant our troponin better. ck-mb, as well, is gonna be another value that we can lookat for cardiac damage. now, last one that we re gonna talk about, it s an importantlab value because it peaks very early at 2
hours, but because its very low specificityto m.i., it s not one that s necessarily used to diagnose m.i., okay? so, that laboratoryvalue is myoglobin. now, what myoglobin does is it helps muscles to use oxygen. okay, sowhen we have this myocardial infarction, this myoglobin is released into the blood streamand it s indicative of this muscle damage, so it s an important laboratory value to have,but because it s not specific to cardiac damage, it s not necessarily as helpful as your troponinsand your ck-mb. and i m gonna tell you most often, in the real world, what you re goingto look at is your troponin. but when the doctor orders cip s or cardiac injury profile,you re gonna run your troponin, ck-mb and myoglobin. okay, so, the questions that youre going to be asked by each of these. which
cardiac markers most, which of these laboratoryvalues is most specific to cardiac damage? boom. that s troponin. which of these ck laboratoryvalues is used for cardiac damage? that s ck-mb, don t forget that. mb, maybe myocardialor something, some way to remember that. lastly, which of these laboratory values is goingto peak the earliest with cardiac damage? that s gonna be myoglobin. okay, so, eachof these 3 values plays a role and that s why we draw them together. but in the realworld, the one that we re going to look at, care about the most is our troponin, specificallyour troponin i. okay. so, let s talk about the symptoms thatpatients are going to have. now, i remember early on as a nurse, i was working in theintensive care unit and i had a patient who
had just gotten in a car accident relatedto alcohol and you know, drunk driving, etc. he s pretty banged up, he d broken his leftshoulder and he was not incredibly verbal. his girlfriend was there and stuff. so, iwas there taking care of him this night and he kept, he started to complain of chest pain,okay, or let me re-phrase that even more. so, he started to complain of pain, so, whathe kinda do is his left shoulder kind of area, and he appeared a little more anxious to me,and so i just... because he had that damage related to that car accident, it was hardto be really diagnose or assess that that might have been from something else. but luckily,i kinda let the doctor know, he s complaining of chest pain, he s very anxious and stuff,so we run an ekg, low and behold, he was in
an active heart attack that moment. and so,we run our cardiac injury profiles, troponins are elevated, and then we begin the, you know,kind of direct interventions for m.i., get them on closer cardiac monitoring, etc., gethim some morphine, we ll get into this in just a minute, we ll get him the whole monaprotocol, morphine, oxygen, nitroglycerin and aspirin. and it turned out well for him,you know, considering, but, being able to assess very quickly the anxiety that the patientis going to have, crushing chest pain, shortness of breath. those are gonna be the 3 thingsthat you re gonna see in these patients. the hard thing is, especially when your patientis not on continuous cardiac monitoring, you re not gonna see, you know, the changes thatare happening. in a hospital, a lot of the
patients are already in pain, they are alreadyanxious, what you re gonna see is people is actually say that there s a weight is on theirchest or an elephant stepping on their chest or just crushing chest pain. those are gonnabe he words that people are gonna use. like, weight, crushing, elephant, just this massivemassive weight that is just right here on their chest that they cannot get rid of. thats gonna be the type of pain your patient is gonna have. if you start seeing your patientexperiencing that, they start becoming short of breath, if they become very anxious, likethis agonizing fear that something bad is gonna happen. that s when you need to, youknow, mention that to a physician, get an ekg done really quick, draw some cardiac injuryprofile, that s all very simple step to do.
you run an ekg in 2 minutes, you can drawthe blood in just a minute and have the lab results back in 30 minutes or so, and be ableto diagnose, yes or no, is the patient is having an heart attack, okay? if they are,we need to treat that immediately. okay. so, if men will also get this kind of left armpain, and not specific to women, they re gonna get a little of pain there too, but this painis gonna radiate on women to the back and to the jaw, okay. and that s on women specifically.so, it can be a little harder to catch this in a woman because they can might be complainingof some jaw pain, and that s not as terrifying necessarily as this crushing chest pain orthey may have some back pain radiated from, you know, the heart. another thing that youmight see is diaphoresis and as well as nausea.
and so, those are the symptoms that you regonna see in your patient as you re assessing them. so, be very cautious and be very astutein assessing your patients. because, like i said, the heart attacks that i have seenpatients have in the hospital or patients that might not necessarily even been cardiacpatients, okay? so, very important to assess very closely. just like we said, immediate treatment forheart attack are gonna be these mona. okay. i want you to remember mona and there willbe a handout here for you to remember this as well. but, mona is the algorithm that sgonna help you remember exactly what to do immediately if your patient is having a heartattack. so, the first thing that we re gonna
do is we re gonna get morphine, we re gonnaget oxygen, we get nitrates, and we get aspirin. okay, so patients that are having heart attack,what each of these things do? well, morphine is given to reduce pain. okay, if they arein severe, severe pain, that s gonna help reduce pain, oxygen, again, we re talkingabout ischemia, right? ischemia means low o2 to muscles, so what we re gonna do withthat oxygen, is because we re dealing with the area of the heart that is not gettingenough oxygen, we get this supplemental oxygen to help reduce that ischemia. so, nitrates,nitroglycerin is what we re talking about specifically here. so what that does is itcauses vasodilation and that is going to reduce the workload in o2 demand of the heart. itwill also reduce o2 demand of the heart. so,
we have this occluded vessel right? so, wegive out nitrates and that s gonna open up our vessel, it cause that vasodilation thathelp blood get through, but it will also decrease the workload of the heart. and on top of that,because we re decreasing our workload, we re decreasing oxygen demand. now, why is thatimportant? well, because we re in, again, because we are in ischemic situation here,and so if we can reduce the amount of oxygen needed for the heart, it can still functionon lower o2 requirements. okay. and lastly, what we re gonna do, is we re gonna give aspirin.what aspirin does is, we know, it reduce platelet aggregation, by doing that, we help a littlebit of blood flow through the little bit of space that we have. okay, so morphine, oxygen,nitrates, aspirin. that s mona.
let s talk about nitroglycerin for just aminute. so, nitroglycerin, we get 1 tablet q 5 minutes, not to give more than 3 tabletsin 15 minutes. the patient should go in 5 minutes, if there is like an angina or something.but if it s not going away, we don t want to give more than 3 tablets in 15 minutes.have them put it under their tongue, it should dissolve, it should help them. they shouldlie down because this gonna cause hypotension due to the vasodilation. okay. now, nitrogylcerin,you can kinda see here in this picture, nitroglycerin comes in a dark container, you need to keepit in a dark container or like a metal container that s sealed off because it can lose itspotency with sunlight, if it s touched too much, they really need to stay in this darkcontainer, not be used unless needed. it should
be carried at all times, there s places thatmake necklaces, they can carry, keep it in a pocket, front chest pocket, and make surethere s some sort of alert bracelet or something that people know if you are having a heartattack, people need to know to be able to give you some nitroglycerin. a tablet shouldbe replaced q 6 months, hopefully you re not going through an entire, you know, bottle.but just to make sure that it maintains its potency, it should change out every 6 monthsor so. alright. so, that s the big points for nitroglycerin. so, now, let s talk about some of the moreinvasive options for treatment with m.i. now, again, we re talking about vascular issue,so how are we gonna fix this vessels. angioplasty
and stent. what is an angioplasty and stent?well, this picture here is a picture of a stent. so, what happens with a stent, is its actually, so here s our patient, so it can actually go into the arm to the heart, orthey can go in through the femoral to the heart. and, what they do, they feed a catheterup there to the spot of occlusion. once they get to the spot of occlusion, they inflatethis balloon, and on that balloon, there s a little wire mesh. so, they inflate this,smash all this junk out of the away push that mesh against the wall, and then they pullthe cord out and so, as you see, blood flow is able to go through here. so, that s thegoal with stenting. for angioplasty, it s very similar except this wire mesh is notleft in there. so, these places are gonna
require anti-platelet therapy, so then weadd something like clopidogrel or aspirin. this is plavix. now, there s other risk factorswith that, of course, but it s important that patient receive this so they can perfuse theirheart. so, we re gonna monitor for bleeding with these patients, they re gonna requireanti-platelet therapy during surgery as well or anti-coagulation therapy during surgeryor procedure. so, it s important to monitor for bleeding. again, we re going in all theway down here, or possibly here, so it s important to monitor this site for hematoma, it s notswelling, it s not becoming hard, there s no under ration and because we re going inthere, that whole sheet is going all the way in there, we wanna keep that leg straightfor 6 - 8 hours to make sure that we have
a good blood flow. another way we can assessfor that, is we re gonna assess distal pulses on the leg, distal to where we went in. so,you ll assess like the foot on the, you know, the right leg, if that s the way they wentin to get to the heart. and they will increase fluid intake on a patient who s like, youknow, we re able to, because what we do during this procedure is we give them dye. and thereason we get the dye is so we can monitor where we re at with our stent throughout theprocedure. so, that s why we get the dye and we wanna increase fluid intake to help youexcrete that dye through the kidneys. okay. one last big treatment that they canhappen here is called cabg - that s coronary artery bypass grafting. what happens withcoronary artery bypass grafting is we take
a vessel, we take a vein from like the leg,and that vein is then surgically inserted into the heart to get, you can see here, its like it s getting the fresh blood here, the blood is coming out of the heart, thisfresh blood, some of it is being shunted back down here to actually perfuse the heart itself.so, this will be like a single bypass, they come in here, so they ll take a vessel fromthe patient s leg, bring it up in here, and then they ll insert, so it s getting freshblood here and then perfusing distal to the area that was being affected. so, that s gonnamake sure that those damaged areas, you can see the damage areas are getting fresh bloodand that they re able to be perfused. okay, so that will be single, double, triple, quadruple.okay, so you heard of quadruple bypass, you
can see how they ve kind of gone it, everysingle one of these, the main coronary arteries, and this is really in extreme cases wherethere s total occlusion and the best option really is just to go in there and create newvascular flow for these parts of the heart that have been affected. okay, so that s kindawhat m.i. is, those are the major things to keep in mind, some of the big treatments.with these patients to go through cabg, of course, they are gonna be at coronary icuafter this, they ll be on ventilator, they ll on fully, and again we re gonna monitorthe activity and monitor their heart rhythm and monitoring for any bleeding after thisas well. okay, so that s kinda big things with m.i., if you have any questions, be sureto ask. i think the next modules, and some
of the handouts and some of the things thatare gonna help you understand more and more. but if you think about it, it s kind of avascular issue, it becomes very easy to deal with. that s all is really is, we have anoccluded vessel, and we have to fix it, and one of the signs, to get rid of that, whatare the cause that and how we re going to prevent it, treat it, and see it in our patients.���������n#p#r#�+�+�+j8l8n8k kk:j