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  • - 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.

- So we know that the most common reason

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心臟病發作(心肌梗塞)病理生理學|NCLEX-RN|可汗學院 (Heart attack (myocardial infarction) pathophysiology | NCLEX-RN | Khan Academy)

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    Hope Bai 發佈於 2021 年 01 月 14 日
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