Health and medicine
- Heart disease and heart attacks
- Stenosis, ischemia and heart failure
- Thromboemboli and thromboembolisms
- What is coronary artery disease?
- Risk factors for coronary artery disease
- Heart attack (myocardial infarction) pathophysiology
- Heart attack (myocardial infarct) diagnosis
- Heart attack (myocardial infarct) medications
- Heart attack (myocardial infarction) interventions and treatment
- Healing after a heart attack (myocardial infarction)
- Complications after a heart attack (myocardial infarction)
Heart attack (myocardial infarction) pathophysiology
Created by Vishal Punwani.
Want to join the conversation?
- Can't the blood push the plaque out the way? I thought the heart was the strongest in your body(0 votes)
- Er... Imagine water washing away at a rock, it would take very long for the rock to erode, right? Similarly, it takes a long time for blood to move the plaque, yet it still grows which becomes an issue.
Hope this helped! :)(12 votes)
- bp 90/40; sat o2 87%; pulse 124bpm; resp 30 bpm, is this an indication of a myocardial infarction?(3 votes)
- Not necessarily. Those vital signs would suggest that things are going badly wrong, but history (if the patient is conscious and coherent), examination, and appropriate tests would be needed to identify and diagnose the underlying cause.(4 votes)
- Is it possible to have 2 heart attacks at the same time? For example, if one large artery was blocked, causing a full thickness infarct, and a smaller artery was blocked somewhere else, causing a partial thickness infarct.(4 votes)
- Sorry this may have been explained in the video, but what is the plaque made out of? Is it like the stuff on your teeth? :)(3 votes)
- The plaque in the blood vessel consists of cholesterol, particularly LDL cholesterol, some fats, white blood cells, and blood vessel wall properties. If you want to find out more, you can check out the previous videos. They go into more detail than my explanation. Hope this helps!(1 vote)
- at10:11what happens if both sides os the cahmbers get blocked?(1 vote)
- For this to happen, it would need both the LAD and another branch from the left coronary artery (for example, the left circumflex artery) to get blocked (bad luck, but possible). In this case, the main problem would also be cardiomyocytes not getting enough oxygen, because of the resulting full thickness infarct. Thus, the contractility of the chamber would massively decrease and would cause an acute left cardiac insufficiency. To learn more, you can watch the video about cardiogenic shock here : https://www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/shock/v/cardiogenic-shock(4 votes)
- What are cardiomyocites?(0 votes)
- They are the muscle cells that make up the cardiac muscle.(8 votes)
- how do you get rid of the plaque in your heart?(3 votes)
- you can't really. atherosclerotic plaques build up over time relative to the amount of insults to the endothelial tissue that are present in the blood stream (carcinogens, for example) as well as the amount of LDL (low density lipoprotein). there's a good video on the development of atherosclerosis here on khan academy in the circulatory system section.
an idea that may at first seem tempting; "to break it down into smaller pieces"; may actually make things worse by loosening fragments that then cause blockages downstream in smaller blood vessels, causing ischaemic infarction in other tissues elsewhere. another issue is that the sclorptic plaque frequently grows an endothelial layer over the plaque which of course makes it difficult to remove.
that said, this sort of technique can be performed during surgery. when it becomes a big problem (patient suffering angina or heart attacks) the main surgery technique that is used is balloon angioplasty, which essentially means putting a catheter into an artery and guiding it into your heart where a a small "balloon" or "stent" like structure supports the coronary artery. modifications to this technique may include something like a "controlled demolition" of the plaque using a small rotary blade at the end of the catheter (rotablation), however, this technique is rarely performed as it found that stents and balloons are associated with long-lasting prognosis.
the best way to avoid the plaques is to not have them start in the first place. of course this is a field of great research and people are researching ways to reduce atherosclerosis, both chemically and physically.(1 vote)
- For a heart attack to occur, does the artery have to be 100% blocked or are there different "levels" of heart attack depending on how much of an artery is blocked? With only partial blockage, can you be having a heart attack or is it called something else such as "Angina"?(2 votes)
- As far as I understood a myocardial infarct level is messured on the ammount of celldeath and not on the blockage of the artery. So I guess the answer to your question is no, there is no need for your artery to be 100% blocked as long as it is blocked enough for there to be enough oxygen deprivation to lead to cardiomyocytes to die. It would be called an Angina Pectoris if the obstruction isn't leading to cell death. And although the level of the myocardinfarct is not messured by the ammount of blockage, there will be a relationship as more blockage will lead to more oxygen deprivation, thus more cariomyocytes dying. I hope that answers your question.(1 vote)
- Would coronary microvascular disease be the partially thickness infarct, and coronary artery disease be the full thickness infarct?(2 votes)
- Why do cardiomyocytes start to burst and leak?(1 vote)
- A myocardial infarction is a blood clot that prevents circulation to the heart muscle. Without circulation, the cell gets no oxygen, so there is a build up of lactic acid in the cells. These cells are contracting 60 times or more a minute and require oxygen to contract, but due to this lactic acid build up, the cells die. You know, if you get a leg cramp when running, you can stop running, increase your oxygen intake, and the cramp will go away as the lactic acid in the leg muscle cells resolves. Without oxygen, cardiac muscle cells die. Dead cells can not maintain their membranes, move electrolytes, or repair and replace molecules. The cells leak and membranes fall apart. When we take blood from the patient we do tests that look for molecules that should be inside cardiac cells such as cardiac specific enzymes. If they are high in the blood, then we know many cells have died. If a large portion in one area of the muscle has died, there will be no electrical conduction through that area and as a result, the tracing of the EKG can also change. Finally if enough of the heart cells stop contracting, no oxygen will be delivered to the rest of the body and the patient dies. Therefore, treatment focuses on breaking down the blood clot in the heart capillaries that started this terrible cascade of events.(3 votes)
- 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.