Myocardial Infarction (MI Heart Attack) for NCLEX Review and nursing students

Myocardial Infarction (MI Heart Attack) for NCLEX Review and nursing students


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 and
it 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 attack
or stents, etc, that you ll have to understand how to take care of them and how to best provide
a appropriate therapeutic nursing care for these patients. Okay. So, very briefly, let s talk about exactly
what heart attack is. So, what happens in heart attack is, blood flow stops to part
of the heart causing damage or death to the heart muscle. Okay, so that s really all heart
attack is. What happens here, you can see, they ve taken this vessel here and they ve
blown it up. So, what happens is, you have this plaque build up and blood clot, and what
that does is it impedes blood flow pass this point. So, of course, once blood can t get
down 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 muscle
dies, 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 allow
that blood to flow and restore oxygen supply to that cardiac muscle. Okay, so when we talk
about 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 a
vascular disorder, okay. Because, what it really is, is we have poor vessels, and because
of 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 of
the main arteries really quick. So, in here we have our aorta coming out. So, coming off
the aorta here, we have our right coronary artery, this kinda come down this way, and
then 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 anterior
descending coronary artery. Okay, so, left main, left main coronary artery, right coronary
artery, 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 distilled
to the occlusion. So, right coronary artery, left main coronary artery, left anterior front
of 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 because
we can actually tell based on EKG where the heart attack is. You know. So, let s, before I get ahead of myself, let
s dig in where we need to dig into. So, as I said, it s really a, it s a very common
disorder, 735,000 Americans have heart attack every year based on the information from the
CDC. 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 Americans
have 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 heart
attack. Now, you can see, it s very regionally distributed here, kind of in our South where
there s more, traditionally more fried foods, more sanitary lifestyles, less active, more
smoking. These are areas that are going to be have higher incidents of heart disease
and 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 something
that 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 why
we re gonna talk about as a vascular. So once we talk about vascular disorder, we re going
to understand how it happens, some of the signs and symptoms we re gonna have, some
of the causes and then the therapeutic interventions that we re gonna be able to do. So, modifiable
risk factors, like we said, smoking, we talked about hypertension. Okay, so, smoking of course
is gonna lead to atherosclerosis and thereby lead to vessel damage. Obesity, as well, you
re 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 vascular
issues and possibly lead to M. I. Hypercholesterolemia, like we said, high LDL, high low density lipoproteins
is going to lead to that occlusion, right? Cause we get that high LDL, we re gonna build
plaque 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 that
vascular damage, those vessels become weak, we may have increased blood sugars more often
and 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 vascular
damage, okay? Now, there s a couple of different types of
M.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. is
gonna be on an EKG. Now, we re gonna be able to see on EKG the ST Elevation, okay, so we
re 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 Myocardial
Infarction and that s a Non-ST Elevation M.I. or NSTEMI. Okay, so on an NSTEMI, you re not
gonna see these EKG changes, okay, specifically the ST elevation. However on a STEMI, you
re gonna notice these EKG changes. And the reason for that is, because, what happens
to cause this ST elevation is that you have complete occlusion, complete occlusion of
a major coronary vessel. Now, once we have that complete occlusion of one of these major
vessels that we talked about a minute ago, we re leading, it becomes incredibly an emergent
situation, 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 then
what happens is, as they develop this complete occlusion of this major vessel, is this S-T
segment 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 any
of this electrophysiological change here, we re gonna see this S and T kinda just becomes
one big wave and that s the ST elevation. Okay. So, that s kinda the EKG change that
you 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 you
what lead you re gonna actually see the change in on your 12-lead EKG. Now, we don t talk
a lot about 12 lead here because it s not necessary for NCLEX. But once you understand
12-lead and kinda understand these EKG changes, you re gonna see, you ll be able to look at
12-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 artery
that is affected. Okay. So, some of the other things that we
re gonna do with a patient who is suspected to have an M.I., is we re going to draw what
is called Cardiac Injury Profile, or CIP s, as what we call them. So, if a patient that
came 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, say
we ll do any CIP s on this patient. Okay, and so, those are kind of 3 major labs that
we 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 re
gonna see most often, looked at and referred to is gonna be your Troponin I, okay? These
Troponin I and Troponin T are found specifically in cardiac muscle, and they re release when
there are cardiac muscle damage, so because of that, it s the most sensitive to cardiac
damage. So, that s one of the questions that you may see on NCLEX is which laboratory value
is most sensitive to myocardial infarction or cardiac damage. And, that s gonna be your
Troponin, specifically, like I said, you re gonna refer to probably most often to Troponin
I. Now, the level of your Troponin is gonna peak at 12 hours. So, what you ll see is when
someone 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 may
stay somewhat elevated though. So, again, Troponin I and Troponin T are the laboratory
values 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 are
2 different kinds of creatinine kinase, you re gonna have creatinine kinase MB, BB, but
specifically for heart damage, you re gonna look at MB. And that might be a question as
well. 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 gonna
be CK-MB. Now, it s found almost, the MB form of CK is found most, almost entirely in heart
muscles, it s release with heart damage as well, its peak time is a little bit longer
though. So, in order to get a more appropriate value, something more specific, we re gonna
want our Troponin better. CK-MB, as well, is gonna be another value that we can look
at for cardiac damage. Now, last one that we re gonna talk about, it s an important
lab value because it peaks very early at 2 hours, but because its very low specificity
to M.I., it s not one that s necessarily used to diagnose M.I., okay? So, that laboratory
value is myoglobin. Now, what myoglobin does is it helps muscles to use oxygen. Okay, so
when we have this myocardial infarction, this myoglobin is released into the blood stream
and 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 Troponins
and your CK-MB. And I m gonna tell you most often, in the real world, what you re going
to 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 you
re going to be asked by each of these. Which cardiac markers most, which of these laboratory
values is most specific to cardiac damage? Boom. That s Troponin. Which of these CK laboratory
values is used for cardiac damage? That s CK-MB, don t forget that. MB, maybe myocardial
or something, some way to remember that. Lastly, which of these laboratory values is going
to peak the earliest with cardiac damage? That s gonna be myoglobin. Okay, so, each
of these 3 values plays a role and that s why we draw them together. But in the real
world, the one that we re going to look at, care about the most is our Troponin, specifically
our Troponin I. Okay. So, let s talk about the symptoms that
patients are going to have. Now, I remember early on as a nurse, I was working in the
intensive care unit and I had a patient who had just gotten in a car accident related
to alcohol and you know, drunk driving, etc. He s pretty banged up, he d broken his left
shoulder and he was not incredibly verbal. His girlfriend was there and stuff. So, I
was 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, what
he 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 hard
to 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., get
him some morphine, we ll get into this in just a minute, we ll get him the whole MONA
protocol, 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 patient
is going to have, crushing chest pain, shortness of breath. Those are gonna be the 3 things
that you re gonna see in these patients. The hard thing is, especially when your patient
is not on continuous cardiac monitoring, you re not gonna see, you know, the changes that
are happening. In a hospital, a lot of the patients are already in pain, they are already
anxious, what you re gonna see is people is actually say that there s a weight is on their
chest or an elephant stepping on their chest or just crushing chest pain. Those are gonna
be he words that people are gonna use. Like, weight, crushing, elephant, just this massive
massive weight that is just right here on their chest that they cannot get rid of. That
s gonna be the type of pain your patient is gonna have. If you start seeing your patient
experiencing that, they start becoming short of breath, if they become very anxious, like
this agonizing fear that something bad is gonna happen. That s when you need to, you
know, mention that to a physician, get an EKG done really quick, draw some cardiac injury
profile, that s all very simple step to do. You run an EKG in 2 minutes, you can draw
the blood in just a minute and have the lab results back in 30 minutes or so, and be able
to 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 arm
pain, and not specific to women, they re gonna get a little of pain there too, but this pain
is 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 complaining
of some jaw pain, and that s not as terrifying necessarily as this crushing chest pain or
they may have some back pain radiated from, you know, the heart. Another thing that you
might see is diaphoresis and as well as nausea. And so, those are the symptoms that you re
gonna see in your patient as you re assessing them. So, be very cautious and be very astute
in assessing your patients. Because, like I said, the heart attacks that I have seen
patients have in the hospital or patients that might not necessarily even been cardiac
patients, okay? So, very important to assess very closely. Just like we said, immediate treatment for
heart attack are gonna be these MONA. Okay. I want you to remember MONA and there will
be a handout here for you to remember this as well. But, MONA is the algorithm that s
gonna help you remember exactly what to do immediately if your patient is having a heart
attack. So, the first thing that we re gonna do is we re gonna get morphine, we re gonna
get 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 are
in severe, severe pain, that s gonna help reduce pain, oxygen, again, we re talking
about ischemia, right? Ischemia means low O2 to muscles, so what we re gonna do with
that oxygen, is because we re dealing with the area of the heart that is not getting
enough 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 it
causes vasodilation and that is going to reduce the workload in O2 demand of the heart. It
will also reduce O2 demand of the heart. So, we have this occluded vessel right? So, we
give out nitrates and that s gonna open up our vessel, it cause that vasodilation that
help 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 that
important? 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 function
on 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 little
bit 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 a
minute. So, nitroglycerin, we get 1 tablet q 5 minutes, not to give more than 3 tablets
in 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 should
lie 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 keep
it in a dark container or like a metal container that s sealed off because it can lose its
potency with sunlight, if it s touched too much, they really need to stay in this dark
container, not be used unless needed. It should be carried at all times, there s places that
make necklaces, they can carry, keep it in a pocket, front chest pocket, and make sure
there s some sort of alert bracelet or something that people know if you are having a heart
attack, people need to know to be able to give you some nitroglycerin. A tablet should
be 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 months
or so. Alright. So, that s the big points for nitroglycerin. So, now, let s talk about some of the more
invasive 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 it
s actually, so here s our patient, so it can actually go into the arm to the heart, or
they can go in through the femoral to the heart. And, what they do, they feed a catheter
up there to the spot of occlusion. Once they get to the spot of occlusion, they inflate
this 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 pull
the cord out and so, as you see, blood flow is able to go through here. So, that s the
goal with stenting. For Angioplasty, it s very similar except this wire mesh is not
left in there. So, these places are gonna require anti-platelet therapy, so then we
add something like clopidogrel or aspirin. This is Plavix. Now, there s other risk factors
with that, of course, but it s important that patient receive this so they can perfuse their
heart. So, we re gonna monitor for bleeding with these patients, they re gonna require
anti-platelet therapy during surgery as well or anti-coagulation therapy during surgery
or procedure. So, it s important to monitor for bleeding. Again, we re going in all the
way down here, or possibly here, so it s important to monitor this site for hematoma, it s not
swelling, it s not becoming hard, there s no under ration and because we re going in
there, that whole sheet is going all the way in there, we wanna keep that leg straight
for 6 – 8 hours to make sure that we have a good blood flow. Another way we can assess
for 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 went
in to get to the heart. And they will increase fluid intake on a patient who s like, you
know, we re able to, because what we do during this procedure is we give them dye. And the
reason we get the dye is so we can monitor where we re at with our stent throughout the
procedure. So, that s why we get the dye and we wanna increase fluid intake to help you
excrete that dye through the kidneys. Okay. One last big treatment that they can
happen here is called CABG – that s Coronary Artery Bypass Grafting. What happens with
Coronary 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, it
s like it s getting the fresh blood here, the blood is coming out of the heart, this
fresh 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 from
the patient s leg, bring it up in here, and then they ll insert, so it s getting fresh
blood here and then perfusing distal to the area that was being affected. So, that s gonna
make sure that those damaged areas, you can see the damage areas are getting fresh blood
and 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, every
single one of these, the main coronary arteries, and this is really in extreme cases where
there s total occlusion and the best option really is just to go in there and create new
vascular flow for these parts of the heart that have been affected. Okay, so that s kinda
what 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 ICU
after this, they ll be on ventilator, they ll on fully, and again we re gonna monitor
the activity and monitor their heart rhythm and monitoring for any bleeding after this
as well. Okay, so that s kinda big things with M.I., if you have any questions, be sure
to ask. I think the next modules, and some of the handouts and some of the things that
are gonna help you understand more and more. But if you think about it, it s kind of a
vascular issue, it becomes very easy to deal with. That s all is really is, we have an
occluded vessel, and we have to fix it, and one of the signs, to get rid of that, what
are the cause that and how we re going to prevent it, treat it, and see it in our patients.
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20 thoughts on “Myocardial Infarction (MI Heart Attack) for NCLEX Review and nursing students

  1. great video – to the point- thank you
    which treatment would you apply first though? im preparing for nclex now but while in nursing school i had a question that was asking what would you give an mi patient with excruciating chest pain ? most of us put morphine but the teacher said it was oxygen. could you please clarify on to what nclex wants? tia

  2. I am a part time student of medical terminology. Thanks a lot for explaining this briefly without using too much jargons.

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