[0:07]What's up Ninja Nerds? In this video today, we're talking about coronary artery disease. This is going to be a part of our clinical science section. If you guys want to follow along and really understand this topic with some great notes, some great illustrations, go down in the description box below, we got a link to our website where you guys can check that out. Also, on our website, we are going to be working on developing a USMLE Step Two and a PANCE prep kind of course. So, if you guys are interested, be on the alert, that'll be coming out pretty soon. Also, you guys like the merch? We got some new merch going on here, check this out. Please go down the description box below and check out the link there as well. Get yourself some swagoo there. All right, we're going to start talking about CAD. So, CAD, diseases of the coronary arteries, what it is. We're not going to go through, we should have already covered this in our basic kind of foundational science concepts about the coronary vascular anatomy. What I really want us to do, to really kind of get straight to the point here, is here we have a section of the heart. So I took, and I cut the heart, and I can see here, parts of the ventricle. So, here's going to be my right ventricle, and here's my left ventricle. This will be the posterior portion, and then over here, coming out of the whiteboard, like it's going to punch you in the face, this is the anterior portion. What happens is you have vessels that are going to supply this big chunky muscle of the actual heart. What are those? Those are the coronary vessels. And the most basic concept, there is four that I really need you guys to remember. One here in the posterior portion, guess what? It's not that hard. It's called the posterior descending artery, we're going to abbreviate that as the PDA. It doesn't take a rocket scientist to figure out that this supplies the posterior portion of the heart. It will supply a little bit of the right ventricle, a little bit of the left ventricle as well. The other one, which is going to be on this right part here, is called the right coronary artery. This one supplies the right ventricle, and parts of the inferior portion of the left ventricle. This right here is the big daddy. This is the Mac Daddy of all the coronary vessels, this is the one that you don't want to get occluded. This is called the LAD, or the Left Anterior Descending Artery. This one supplies the septum, it supplies the anterior wall of the left ventricle, and it even gives off some of the lateral wall of the left ventricle. So, really, really important artery. And the last one here that we have that we're going to zoom in on in just a second here, this one is called the Left Circumflex Artery, which we're going to abbreviate LCX. And that supplies the lateral wall of the left ventricle. So, when we talk about coronary artery disease, it's a disease of these vessels. So, we have to zoom in on a chunk of this vessel and the associated myocardium, that's what we're going to do here. So, we're zooming in on this puppy, so this is a zoom in view of that that portion there. So, here we're going to have a portion of the the left circumflex artery, and here's a piece of myocardium. What happens in patients who have coronary artery disease is the most common cause of that disease is atherosclerosis. That is by far the most common cause. So, then we have to ask ourselves the question, what is atherosclerosis and what causes atherosclerosis? Atherosclerosis is these fatty plaques that develop within the wall of the actual blood vessel and occlude the actual blood flow. What leads to this? I want you to remember the mnemonic "sad CHF". So, sad CHF will give you the following things to remember. One is smoking. Second is advanced age. Now, when I specifically talk about this one, I'm talking about greater than 45 for males and greater than 55 for females, don't forget that. D, got the diabetes. The C is for cholesterol. So, this one's a kind of a funky one, right? So cholesterol is high. Now, when I talk about cholesterol being high, which ones am I specifically talking about? This is the real problem here. There's two of them. It's high LDL and then a weird one that kind of doesn't completely go along with this, is low HDL. So, don't forget that as well, so a dyslipidemia. The next one is hypertension. And finally, a family history of coronary artery disease. So, these particular risk factors will then do what? It'll stimulate this vessel to become diseased. It'll cause plaques to form within the actual coronary vessel. Now, when that happens, look what we get, we can get two particular scenarios here. You see this vessel here? Now, look, you got this big old atherosclerotic plaque. The big difference here is that this is called stable coronary artery disease because what happens is, the plaque is kind of covered by this fibrous tissue. And the interesting thing about this plaque is that it's very stable, but what you will notice is that, look at the lumen, in comparison here, the lumen is significantly smaller. So, because of this, what's going to happen to the actual blood flow in this particular area here, there's going to be a reduction in the oxygen supply. If I have a reduction in oxygen supply because of having this big old stenosis, a luminal stenosis of the coronary vessel, that's going to lead to less oxygen being delivered to the myocardium. Now, that may lead to ischemia, but generally these patients don't have a lot of ischemic symptoms, the chest pain is the primary classic finding. What really leads to this is something else. This myocardium decides to say, all right, you're giving me a very little oxygen. But what if, for some reason, I decide to consume more oxygen? That's interesting. So, what will be a reason why the patient would decide to have an increase in the oxygen consumption? Maybe they're demanding more, let's use that term. So, there's an increase in the O2 demand. Now, the reason for the reduced O2 supply is this plaque. This plaque is causing the reduced oxygen supply. What would be causing the increase in oxygen demand? There's two particular reasons that I want you to think about. One is the patient's heart rate decides to go through the stinking roof. They decide to take away, maybe in the 170s, 180s, whatever it may be, that's causing the heart rate to go up. If the heart rate goes up, the heart has to beat faster, it has to work harder and consume more oxygen. If the demand goes up and the supply is low, you create a mismatch and a recipe for ischemia. So, that's one particular reason, so if we have these two particular things here, this is a recipe for what? Ischemia. And what is ischemia? Ischemia can be simply defined as a reduction in perfusion to the tissue and an inadequate to meet the tissue's demands. So, that's the big stimulus here. Now, what's another reason why the O2 demand can go up? Another one is high blood pressure. If the patient has hypertension, they decide to shoot their blood pressure up. So now their afterload is crazy high. If their afterload is crazy, crazy high, now the heart is going to have to beat so much harder to generate enough stroke volume to push blood out of the heart. That's the big concept here. And so, this is why this is so interesting and because in patients who have stable coronary artery disease, when they're at rest, they don't really have any angina. What really starts to happen is when they start to exert themselves and increase their oxygen demand, then they develop angina. And so, one of the classic findings of CAD is that in these patients, they have ischemia. But generally, this ischemia, what's the way that they'll present? They'll present with angina. So, let's actually do this in red here because this is the classic finding of patients who have stable CAD. But this angina is very, very specific. In the sense that the angina will only actually do what? Increase or occur whenever the patient is exerting an increase in their demand. And so, this is angina that is worse with exertion. Because if you exert yourself, you decide to go running, you decide to walk or you whatever it may be, you increase your heart rate, you increase your blood pressure, you increase the demand. Then if you decide to decrease the demand, you stop exerting yourself, what would happen? The demand would go down and the ischemia should actually go away. So, this would get better with rest. This is generally the classic finding of patients who have stable CAD. They have a stable plaque reducing supply if you increase their demand. This will cause worsening ischemia. All right. Next, next concept here. This is the scary one, this is the one that most people are frightened of in CAD. They have a diseased coronary artery, right? We're just using this left circumflex as an example. They have a plaque. Maybe the plaque is somewhat stable, but it's not completely stable, at certain parts. And what happens is this plaque decides to rupture. So you get what's called a plaque rupture. And why is that bad? Well, if you rupture that plaque, you expose that inner cheesy material, which is highly thrombogenic. When it's extremely thrombogenic, what happens here? When you have this massive plaque rupture, platelets love to come and stick to this and then you develop this thrombus. Oh my gosh, that's terrifying. So, you have a plaque rupture and this creates a thrombus that forms on the actual plaque. When you have a thrombus that forms on top of the plaque, now what happens to your O2 supply here? It's massively decreased. And so, what happens in these particular patient populations is their O2 supply is incredibly low. And if you have an incredibly low O2 supply, you're going to stop perfusing the myocardium. And the myocardium here is going to start becoming ischemic. And that's the scary part of acute coronary syndrome. But we have to be able to differentiate these because they're a tiny bit different in nomenclature and understanding the actual disease process. So, let's say here I take three particular types of acute coronary syndromes. In one scenario, I rupture the plaque. When I rupture the plaque, it does kind of really kind of bust open, a lot of this thrombus starts to form. And then same thing here for NSTEMI. I rupture the plaque, a lot of thrombus begins to form. So, we call this what? For these two, this is a subtotal occlusion. Now, when I have a subtotal occlusion, because I form this this thrombus on the plaque, then I'm reducing the blood supply very, very significantly, right? So, definitely for both of these, I'm going to have a reduction in O2 supply, very, very low O2 supply. But the big primary difference here is what happens to the myocardium. Now, you're not giving enough oxygen to the tissue. In this particular scenario, if I have the patient having ischemia of their subendocardial layer, so I have what's called subendocardial ischemia, that is more specific for unstable angina. So, this is going to be again, a subendocardial ischemia. And here is the big, big difference. I reduce the supply, my subendocardial layer begins to start screaming. But here's the other thing, I don't kill any tissue. None of the tissue dies. And so, there is a particular molecule that leaks from these tissues whenever there's tissue death. Do you guys know what that's called? Troponins. I know you guys are all screaming at home, right? So, troponins. What would I say about the troponins? Would they be positive or negative? They should be negative. Right? So, that should be one particular thing. And on top of that, what we'll learn a little bit later is, is they shouldn't have any ST segment like elevation. They may have because of this ischemia, they may have what's called some ST segment depressions or some T wave inversions. And that's the other thing that we'll actually remember for these two. But we'll go over that when we get into the diagnostic section. Now, you're probably like, okay, these are kind of the same though. Zack, he said a subtotal occlusion for both of these. So, what's the difference between unstable angina and NSTEMI? Well, really with an NSTEMI, I actually have my supply so low that I actually began to infarct. So, it's no longer subendocardial ischemia. This is called a subendocardial infarct and that is the big difference here. I actually am causing death of the tissue.
[12:58]If there is death of the tissue, what will leak out as a result? Troponins. And so, if the troponins are leaking out, they should be positive if we were to test them. So, we will have a positive troponin. And the last thing is, is this is a small infarct. It doesn't cause ST elevation, but it does cause ST depression or T wave inversion. And that is how we really kind of differentiate between these two when it comes down to the pathophysiology.
[15:04]The last thing, the last thing that I want you guys to understand here, is for stable CAD, they present with angina, worse with exertion, better with rest, because it's particularly exertional dependent. For acute coronary syndromes, their type of angina is a little bit different. For these guys, for the acute coronary syndromes, these guys present particularly with angina.
[15:32]Same thing, same thing, but this can occur at rest, and it is more intense. So, there's an increase in intensity of that pain, it is much, much more intense, and there is an increase in frequency of the pain. So, when you're trying to compare the two between an acute coronary syndrome angina and a stable angina, this is really the big difference. If it occurs at rest, it's intense and it's occurring more and more frequently, that's more concerning for an acute coronary syndrome. If it's an angina that occurs with exertion and improves with rest or what we call nitro, which we'll talk about in the treatment section, that's stable angina. The other thing that I want to talk about really quickly is this classic finding of angina, if you will. So, when patients present with angina, it is a substernal type of chest pain, it's a squeezing, choking type of pain. And generally, this can, you want to watch out for, radiate to the left neck, left face, left arm. All right. Other associated symptoms that can be atypical findings or anginal equivalents is epigastric abdominal pain and some nausea and diaphoresis, so watch out for that. All right, let's now take this understanding that we have of the pathophysiology and move into what happens if a patient does infarct, they damage their myocardium. What are some issues or complications that can arise? All right, my friends, so now the patient has come in, they have developed an NSTEMI or a STEMI, so they have infarcted some of their tissue. When a patient has infarcted some of their tissue, you're going to start seeing potential issues and complications arise. What are those issues? What are those complications that we have to be wary of because it can have a high mortality rate? So, one of the big things is when you start to infarct the tissue, it can increase the risk of arrhythmias. Arrhythmias usually develop within the first 24 hours after a patient has had some type of NSTEMI or STEMI. So, this is the one that you want to watch out for very early in that course. What can happen is, one of the things that you can actually see here is, you know whenever patients develop what's called a RCA occlusion, right? So, they develop what's called a right coronary artery occlusion. Do you guys remember which parts of the heart that supplied? I'm pretty sure you're going to get it right. The right ventricle and inferior aspect of the left ventricle. But another thing is it gives like this little branch that supplies the AV node. And sometimes in patients who get these RCA occlusions, you can actually destroy this structure here. So, here's you have your AV node, and you go into your bundle branches. I can actually destroy this structure here. And if I have an RCA occlusion that leads to an AV node destruction, now what's going to be the problem with that? This is supposed to be able to allow for electrical activity to go from the atria into the ventricles. Now, you lose that. You're going to start developing AV blocks. And so, this patient could develop a AV block that could precipitate a profound bradycardia. And so, this is something that you want to watch out for, watch out for like second degree heart blocks, third degree heart blocks. This is something that can be potentially evident. So, if the patient is developing an RCA occlusion, this RCA occlusion could potentially cause AV node destruction, which could then lose the electrical connection between the atria and the ventricles, precipitating an AV block, and now the actual infra components or like the Purkinje system now have to take over the actual rate of the heart. And that will lead to a profound bradycardia. All right, so that's one thing to watch out for. So, if you have a patient who is then had an NSTEMI or STEMI, check potentially if they have bradycardia, you really want to watch out for that as a potential complication. The other thing that can happen, and you usually see this with any kind of like LAD or left circumflex kind of occlusion. This is usually going to affect the left side of the heart. So, whenever these patients actually develop an infarct, they start to damage this left ventricular tissue. And whenever you damage this left ventricular tissue, you infarct it, now you create a reentrant circuit. So, LAD left circumflex occlusions can increase what's called reentrant circuits. The problem with that is, is that if you create reentrant circuits within the ventricle, this can create a ventricular rhythm, and that is absolutely terrifying. Because you know what these patients can potentially develop? If they develop this reentrant circuit, then starts flying off these kind of electrical activities, the patient can potentially go into what's called ventricular tachycardia. That could potentially go to ventricular fibrillation, and then from there, sudden cardiac death. So, you really want to watch out for these potential complications in patients who have developed an NSTEMI or STEMI. And again, just to remind you, when is this the most profound? Usually, you want to watch out in the first 24 hours after an NSTEMI or a STEMI for particular types of arrhythmias. All right, so these are the two big ones that I want you to remember here. The next really, really scary one that you can't miss, and again, this is usually most common in the first 24 hours as well, is acute heart failure. This is one of the big causes of acute heart failure. So, with arrhythmias, particularly V-tach, V-fib, because you can cause a ventricular arrhythmia or cardiogenic shock from a really nasty infarct. If that happens where there's hemodynamic or electrical instability, they need to go to the cath lab because the cause of their instability is the occlusion.
[21:32]And the last thing is you can add them on statins as well. Statins help to prevent the actual plaque from continuing to hopefully get bigger and bigger and bigger. We don't want that. So, again, standard therapy, aspirin, beta-blocker, nitro sublingual, PRN, isosorbide dinitrate for long-term control, beta-blockers if need be. Add on the statin, they're still symptomatic, angiogram shows high risk lesions. The stress test is really bad, revascularize them. PCI based on this, CABG based on this. If they get the stent, they need dual antiplatelet therapy for a year. And that, my friends, covers coronary artery disease. I hope you guys liked it, I hope it made sense, and I hope it helped as always, until next time.
