Heart attack (myocardial infarction) pathophysiology | NCLEX-RN | Khan Academy

– So we know that the most common reason heart attacks happen is because of atherosclerotic plaque build-up that happens in your coronary ateries. And this plaque build-up will compromise blood flow to your heart muscle. And when your heart muscle doesn’t get access to blood flow, it doesn’t get access to
oxygen inside that blood, so that’s essentially how
you get a heart attack. And remember, in medicine,
we call heart attacks myocardial infarcts. So myocardial referring to muscle, muscle of the heart, and infract referring to lack of oxygen causing death of tissue. So myocardial infarct, lack of of oxygen to heart muscle causing death of that heart muscle. That’s what a heart attack is. So we know how a heart attack occurs. But what exactly is
happening in your body? What’s happening with your heart when you’re actually
having a heart attack? Well, let’s take a look at that. And let’s actually start
from the beginning here. Let’s bring in an artery here so we can visualize what happens to the heart muscle cells
during a heart attack. So here’s our artery. So let’s draw in our cells now. So there are some heart muscle cells. And so you might have noticed that I drew these cardiomyocytes in a really oddly connected way. So you can see a connection there, and you can see connection there, and there’s one there, and so on. And the reason that cardiomyocytes, that heart muscle cells
are connected in this way, is because by being connected like this, they can more efficiently work together to make sure that the
heart pumps properly. So what exactly is
happening in a heart attack? So let’s say we’re looking
at this blockage right here. And then let’s say the piece of artery that we’ve drawn is this piece of artery right here. So all of these cardiomyocytes here, all these cardiomyocytes are what’s surrounding this vessel here, all right? So it’s this piece right
here that we’re representing. So you’ve got this plaque
in your artery upstream, and it’s not ruptured,
it’s just sitting there. It’s not really doing too much right now. But then let’s say you start
playing soccer, all right? So you start running around,
chasing after the ball, and when you’re running around, blood is being forced to sort
of flow faster and faster through your coronary arteries, right, because your heart’s pumping faster. Well, all of that blood sort of rushing through your coronary arteries because your heart’s pumping faster, that rushing blood will
sort of bombard your plaque, and your plaque might rupture. So let’s say it does rupture in this case, and you develop this thrombus. So you develop this big clot
on that ruptured plaque. Well, in this case, what do you think is going to happen to the downstream part of that artery? It’s not going to get
that much blood, right, because this thrombus is
blocking off the blood flow. So whereas before you had lots of blood flowing through your coronary artery, and therefore your cardiomyocytes were getting lots of
oxygen out of that blood, now, because of that huge
clot that’s in the way, there’s way less blood flow in that coronary artery, right? Blood flow to that heart muscle there starts to slow down. So now all of a sudden
these heart muscle cells aren’t really getting all
the oxygen they need, right? So now they start to
become oxygen-starved. They start to get really
hungry for oxygen. And when they get really
hungry for oxygen, they start to send pain
signals to the brain. And these pain signals are
basically telling the brain, “Brain, we’ve got like
no oxygen down here. “You need to do something about this now.” And actually, this pain can feel a bit like indigestion, because you’re not really
used to pain like this, so your brain kind of gets confused and thinks it’s maybe an indigestion pain. So you might actually feel the pain just below your heart,
right above your stomach. So this is actually the
start of a heart attack. So let’s look at our clot now. Well, it’s actually still growing, and it’s now blocking like
two-thirds of the artery. So your pain will start to get worse. And some people might start to get pain in their arms, and mostly we see it in the left arm, and the reason you can
get pain in your arms in the first place with a heart attack is because some of the nerves that are connected to the heart have the same origin as some of the ones that are connected to your arm. So since your brain really isn’t used to feeling pain from your heart, it sort of gets confused when it does get signals from your heart. And in that confusion, it thinks the pain is
coming from your arms. And that’s called referred pain. So it’s kind of a similar mechanism to the indigestion feeling. And by the same referred pain mechanism, some people even get pain radiating up to their jaw. And so at this point, the brain is confused, right? I mean, it’s overloaded with these increasing pain signals coming from the heart, right? And to add to that, you’ve got all of these cardiomyocytes that are running low on oxygen. And because they’re running low on oxygen, the nice, normal, coordinated way that your heart beats will be compromised. And your brain doesn’t like this, so your brain senses this, and says, “Holy crap, I need to do
something about this.” So your brain triggers this big surge of adrenaline release
into your bloodstream. And the adrenaline gets everywhere, so it gets to your heart, and it starts affecting your heart, right? And what does adrenaline do? Adrenaline will start to make you heart beat faster. Your heart will start to race. Unfortunately, the adrenaline’s
not going to be able to do anything about the
clot that’s built up, which is actually just growing, right? I mean, we’ve sort of
left it alone for a while, but it’s actually getting bigger. And by now it’s filling up
basically the whole artery. It’s completely blocking the artery off. So now our cardiomyocytes
are in big trouble, because now they’re
barely getting any blood, so they’re barely going to get any oxygen. And because they’re
barely getting any oxygen, they necessarily have to slow down their rate of contraction, because having good access to oxygen is really key for cardiomyocytes to produce the energy they need to do all the work they have to do. So, naturally, if they
don’t have that oxygen, they can’t produce all
of the energy they need, so they have to slow down. So they start to slow down, and then they start to
stop beating altogether. So because our patch
of cardiomyocytes here have stopped beating, well, the rest of the heart has to compensate. So the rest of the heart
starts beating faster to compensate for our dying
patch of cardiomyocytes. Now, at this point, this
are not looking good for our cardiomyocytes. They actually can’t even hold themselves together
in one piece anymore. Their membranes actually
start to break down, and the cells start to rupture. See, cells without oxygen,
without blood supply, they don’t get the luxury of having blood carry away their toxic waste products that sort of naturally crop up as part of their regular metabolism. So these toxic waste products start to build up inside of our myocytes, and their membranes start to rupture. Now, when our cardiomyocytes
start to rupture, they start to leak proteins that only heart muscle cells contain. They start to leak these proteins into the bloodstream. These proteins are called troponins. Troponins are a type of structural protein that you only find in heart muscle cells. So keep that in mind, because that’ll become important later on when we talk about
diagnosing heart attacks. And so now our injured heart is really starting to wear itself out, and the beat is starting
to get a bit weaker, and you’re starting to
get even more effects all over your body. For example, it’ll start to become really difficult to breathe, because you can actually get some fluid built up in your lungs. And let me just quickly
show you how this happens. So here’s your heart,
and here are your lungs. Now, remember, blood
goes out from your heart to your lungs to get oxygenated, and then once it gets oxygenated, it sort of comes back
to your heart, right? And then it gets pumped out of your heart to the rest of your body. Well, when your heart
isn’t pumping very well, blood will sort of build up in your heart and then back up into the lungs, and this buildup, this backflow of blood can end up making it really difficult for you to breathe. So you’ll often get dyspnea, you’ll often get shortness of breath when you’re having a heart attack. So you’ve had your referred pain, you’re getting your shortness of breath, your heart is racing. Well, because your heart
is not pumping efficiently, not enough blood might
be getting to your brain, so you could start to get
dizzy and disoriented. So by now, it’s been
about 15 to 18 minutes since you started having
your heart attack, and now things are getting
really, really bad. Your starving heart muscle cells will actually being to burst and die. They’ll actually being to escalate from just leaking to actually dying. So I’ll draw in some dead faces here. But, you know, this is really serious. If you’re not treated
within about 20 minutes, your heart’ll get damaged so badly that it won’t ever beat normally again. Because at this rate, about 20 minutes after
your heart attack comes on, you’re losing about 500 cardiomyocytes, 500 heart muscle cells per second. Per second. And they’re not like
your average skin cell or your hair, your strand of hair. They can’t actually be replaced. So once you lose these cardiomyocytes, that’s it. Your heart will not beat normally again. So you really want to limit the amount of cardiomyocyte
loss that happens. So that’s sort of the physiology behind what’s happening
in a myocardial infarct. So before we finish up, there’s just one more
thing I want to show you. So we classified myocardial infarcts into two main groups, and I’ll show you those groups. I’ll show you how we divide them up. So what I’m going to do to show you this is we’re going to take
a cross-section here across the heart muscle, ok? I’ll draw that cross-section. So this is a cross-section of the heart. So it’s sort of as if we cut away this part on the bottom here and we’re looking upward at the heart. That’s a little eye there. And so this is the right
ventricle on this side, this is the chamber of
the right ventricle, and on this side is the
chamber of the left ventricle, all right, because the
left ventricle is here, and the right ventricle’s over there. Now let’s draw in our blood vessel. So let’s say that right here, all right, I’ll draw a circle, because remember, we’re cutting the left anterior descending artery, this one here, we’re cutting that in
cross-section as well. Left anterior descending artery. So let’s say we block off this left anterior descending. Let’s say that we’ve had a heart attack involving that artery. Well, because it serves such a huge part of the heart wall, what’s going to happen is we’re going to knock off a
big part of the heart wall. We’re going to knock
off a huge chunk of it. Right? And so this type of infarct is called a full-thickness infarct, because it involves the entire thickness of the thick, muscular wall of the heart. So that’s called a full thickness infarct, or a transmural infarct. And transmural, by the way, just means, mural refers to wall, and trans means just sort of crossing. So transmural means it’s just
crossing the entire wall, that’s how big the infarct is. Transmural. So that’s one type of heart
attack. That’s one type. And the second kind, let’s put it up here, the second kind is called a partial thickness, a partial thickness infarct, or a subendocardial, that’s
the other word for it, subendocardial infarct. Well, how does that happen? Well, that happens because you’ll have these little arteries that come off of the big ones. So, for example, there
will be this little one that comes off of the
left anterior descending, and it will actually penetrate through the heart muscle wall, right? Because the goal of this artery is to supply blood to this
little patch here, ok? So let’s say that the supply zone, the oxygen supply zone,
the blood supply zone for this little penetrating artery is this area here. Well, let’s say that you
get a clot that develops in this artery here. Then you’ll still have a heart attack, you’ll still have a myocardial infarct, but it’ll be one of a much smaller region. It won’t actually be a full thickness, it won’t be a full thickness infarct, it’ll just be a partial thickness. So those are the two major types of myocardial infarcts.

40 Replies to “Heart attack (myocardial infarction) pathophysiology | NCLEX-RN | Khan Academy

  1. Your message is so loud and clear, it makes it so much easier for everyone to understand MI pathophysiology. My husband now fully understands how MI occurs and he will make sure he doesn't promotes his partial thickness MI to full thickness MI. thanks

  2. at 6:49 you say troponins are only found in heart muscle cells, which is definitely false, they are key in skeletal muscle as well.  It may be worth overriding the audio to prevent student confusion.  Overall though, very helpful video
    -a grateful MS1

  3. I'd love to see your explanation about MI caused by #SCAD.
    I had 2 heart attacks due to this rare condition where your arteries dissects forming a flap and blocking blood and oxygen flow to the heart. I'm only 43 years old otherwise fit and healthy
    So little is known about this condition, there is no way to prevent it as the causes still unknown and therefore there is no specific treatment either

  4. is it true that subendocardial coronary artery blockage cause non ST elevation Miocardial Infarct , while endocardial coronary artery blockage cause Miocardial Infarct with ST segment elevation?

  5. The plaque here is shown to be in the lumen of the vessel, later allowing the thrombus to attach to it. That's not really the case, the plaque builds up in the subendothelial layer, and increasing force/pressure in the vessels (after exertion) causes the layer (fibromuscular cap) between the plaque and lumen to rupture leading to bleeding inside the vessels, and activation of the coagulation pathway, with a thrombus being the end result.

  6. Regardless of the troponins debate, this was absolutely fantastic! Not only did it explain with great and precise accuracy what one feels/experiences during a AMI, it did a great job of explaining the internal happenings. Thank you

  7. its all stupidly easy but we dont think of how .. we dont care if this does make sense or not
    we just care about As
    and thats exactly what modren universities want .. u pay us .. u come dump doctor or medical personnel

    im really afraid to ask 1uestions hat rushin my head about everything i study
    coz that makes me annoying

  8. I had a clot burst out of the artery in 2011. The Dr told me not many ppl live after having this. I was fully awake. I was only 33.

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