Coronary Artery Disease | Clinical Medicine

foreign 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 US Emily step two in a pants prep kind of course so 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 CD diseases of the coronary artery is 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 be supplying 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'll 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 Mack 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 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 in 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 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 include 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 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 that's 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 current 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 aluminal 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 huh that's interesting so what would 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 tack 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 it's inadequate to meet the tissues 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 they're afterload's 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 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 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 neck next concept here this is the scary one this is the one that most people are frightened of in CAD they have a disease 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 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 as chemic and that's the scary part of acute coronary syndrome but we have to be able to differentiate these because they're a Teensy 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 sub total occlusion now when I have a subtotal occlusion because I form this this rhombus on the plaque then I'm reducing the blood supply C 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 sub endocardial layer so I have what's called sub-endocardial ischemia that is more specific for unstable angina so this is going to be again a sub endocardial ischemia and here is the big big difference I reduce the supply my sub-endocardial 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's a particular molecule that leaks from these tissues whenever there's tissue death you guys know what that's called troponins I know you guys are all screaming at home right so troponins so what would I say 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 they shouldn't really have a troponin bump 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 Zach you said a subtotal occlusion for both of these so what's the difference between unstable engine and stemi well really with an in stemi I actually have my Supply so low that I actually began to infarct so it's no longer sub-endocardial ischemia this is called a sub endocardial infarct and that is the big difference here I actually am causing death of the tissue 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 leak and the last thing is is this is a small infarct it doesn't cause St elevation but it does cause SC depression or T wave inversion and that is how we really kind of differentiate between these two when it comes down to the pathophysiology the last one here is going to be for the stemi and for the stemi this one is primarily a total occlusion a complete total occlusion of that entire coronary vessel so this vessel is completely jacked up it is filled to the brim with clot if I completely clot off this entire Lumen do I have any blood supply no and so the difference between these is that these have very little Supply this one's completely choked off there is zero O2 Supply and if I get no oxygen supply to The myocardium what begins to happen it gets ticked off and the entire myocardium begins to become damaged and because the entire tissue is damaged we call this transmural this is a transmural infarct the entire wall gets jacked up that's no bueno what would happen to the troponins through the roof these usually will bump pretty high and then the last thing is this will definitely present with ST segment elevation that's where we get the name so we'll see particularly ST segment elevation we'll get into the details of that a little bit later but they should have a positive troponin because of the transmittal infarct St elevation because of the transmeral infarct and that is how we pathophysiologically describe semi the last thing the last thing that I want you guys to understand here is for stable CAD they present with Angela 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 acute coronary syndrome findings these guys present particularly with angina same thing same thing but this can occur at rest and it is more intense so there's an increased 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 more frequently that's more concerning for an acute coronary syndrome if it's an engine that occurs with exertion and improves with the rest of what we call Nitro which we'll talk about 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 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 weary 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 developed 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 have develop what's called a right coronary artery occlusion do you guys remember which parts of the heart that's applied it's pretty sure for 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 the patients develop an RCA occlusion this RCA occlusion could potentially cause AV no destruction which could then lose the electrical connection between the Atria and the ventricles precipitating the AV block and now the actual infra uh nodal components or like the purkinje system now have to take over the actual rate of the heart and that will lead to a profound beta bradycardia all right so that's one thing to watch out for so if you have a patient who has 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 Circ kind of occlusions 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 re-entrant circuit so LED left circumflex occlusions can increase what's called re-entrant circuits the problem with that is is that if you create re-entrant 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 and 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 and patients who develop an end stemi or stemi and again just to remind you when is this the most profound usually you want to watch out and the first 24 hours after an end stemi 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 tag v-fib or profound AV blocks like bradycardia you want to think about myocardial ischemia from acute heart failure you want to think about myocardial ischemia as well think about it it's pretty straightforward let's see here we have the left ventricle and then I decide to develop a let's say a massive lad occlusion you can get this from your your left Circle but I'd say the left of the lad would probably be the most disastrous one to have because it supplies the septum the Apex and even a part of the lateral wall you imagine knocking this thing out oh my gosh that'd be terrifying so if you infarct this entire tissue what are you going to do you're going to drop the contractility now now you've caused damage to multiple myocardial tissues you drop the left ventricular contractility you're going to drop the left ventricular ejection fraction if you drop the left ventricular ejection fraction now you're not getting blood out of the heart so the problem with this is is that if I damage this tissue I'm not going to be able to get blood out of the left ventricle and out into the aorta this process is going to be inhibited so there's going to be a drop in what's that called the volume that gets pumped out of the heart within one minute microtic output so my cardiac output will drop then I won't perfuse tissues if the cardiac output drops enough what's that formula blood pressure is equal to cardiac output times the systemic vascular resistance if my cardiac output goes down enough it can potentially drop my blood pressure so the patient may develop hypotension but the most worrisome complication here is if that hypotension leads to reduced perfusion to the tissue it can put a patient into what's called cardiogenic shock so this is when they're not perfusing the tissues and you want to watch out for like potentially multi-system organ failure other organs are going to start failing such as the kidneys right and that's a really really big thing to watch out for so again because you lose you have this led occlusion you knock out a big portion of the left ventricular contractility you reduce the left ventricular ejection fraction and what happens is that drops the cardiac output that can lead to hypotension and can stimulate a patient going into cardiogenic shock so you really want to watch out for this a reduction in contractility a reduction in left ventricular ejection fraction then precipitating this low cardiac output and cardiogenic shock here's the other scary thing if the blood can't go forward so you have a problem getting blood going forward where will it go then what happens is the blood will start backing up into the left atrium and when it backs up into the left atrium it'll go back into your pulmonary circulation when it goes back into the pulmonary circulation where do you think it's going to go it's going to go right into the lungs my friend and then what's going to happen is you're going to start filling the lungs with fluid because the hydrostatic pressure and the pulmonary veins are going to start increasing and fluid is going to leak out and these patients will develop a profound pulmonary edema so you want to watch out for these patients developing pulmonary edema and this can lead to hypoxia so if you have a patient who has just had an instamy or stemi they now are developing features of pulmonary edema such as dyspnea or watch out for that as well they can also develop not just profound hypoxia but they may develop dyspnea so watch out for dyspnea as well or hypoxia so if you have a patient who has an nstemi or stemi massive LED occlusion they knock out the actual contractility they lose their left ventricular ejection fraction they don't pump blood out so develop hypotension and perform perfusion to the tissues and pulmonary edema this is something that you want to think about as acute heart failure and a patient who's had an MI all right that's this one very very scary one you really want to get on top of that one the next one is pericarditis this one is actually one of the nice ones like if you wanted to get any complication this is probably the ones you want to get because this is the one where it's not going to have a super high mortality rate it's not fun I don't want to deny that but it's not going to be the scary one so if you develop an infarct generally anywhere near the pericardium you're going to have infarction of tissue right neutrophils macrophages will all come into this area and try to clean it up and lay down some granulation tissue but there's going to be a lot of inflammation in this area it's not out of this world to think that the inflammation will extend to the nearby pericardium and if it extends to the nearby pericardium this can cause inflammation of the pericardium which will lead to pericarditis now when patients present with pericarditis they present with what's called a pleuritic that's one of the big differences here so sometimes what gets scary and hard to suss out with these patients is they had an MI they came in because they presented with chest pain now they're presenting with chest pain again you have to be able to differentiate the two is it squeezing is it choking is it feel like there's someone sitting on your chest kind of pain radiates to the left jaw neck arm or is it this type of pain where it's a kind of more of a pain that hurts whenever you're taking breaths does it actually change whenever you kind of lean forward a little bit and offload the pressure on the pericardium so there's a positional component of it that's more suggestive of pericarditis another thing is that you want to listen because if the pericardium gets really really inflamed the layers start kind of actually rubbing up against one another and it creates a weird rub on auscultation we call it a friction rub we call it a friction rub and so generally in patients who have low grade fevers a pleuritic chest pain a positional type of chest pain another one great for your boards is a chest pain that radiates to the trapezius that's classic in your vignette so don't forget that one as well but if her presents like this after having some type of cardiac event you definitely want to think about pericarditis now sometimes and I and I hate it we start thinking could there be another component to this like there's two different types of pericarditis this is called fibrinous pericarditis right so there's two types one is called fibernous and the other one is called dresslers how do I suss out the two amphibians pericarditis it's usually very soon generally one to three days after having the cardiac event so that's one thing so if you have a patient who's approximately one to three days post MI it's more likely februinous for your exams in True Life this isn't truly that important but if it's free exams dresslers is usually a little bit later so it's a kind of pleuritic chest pain with a friction rub that comes generally about 14 days two weeks after an MI so approximately two weeks post am I and that's one of the things that they may try to trip you up on your exam in true life it's not that important but for your exams something to not forget about all right so we've got a rhythmias we got acute heart failure we got the pericarditis we come down to the ones that usually cause sudden hemodynamic collapse and these are terrifying as well these I'd say are less common in the new reperfusion era which we have PCI is the primary way that we reperfuse people but complications that can arise and a patient who gets an LED occlusion all right so an LED occlusion what happens is is one of the parts that can get really jacked up here is the interventricular septum so whenever there is a infarct of the interventricular septum you damage this tissue so now look this endocriticular septum is all jacked up it's all infarcted what can happen is sometimes when the tissue is super weak and a chronic it can actually be thin enough that you can rupture the septum and you can create what's called a ventricular septal defect and look at this now when I rupture this puppy I have a big hole in between the left ventricle and the right ventricle and generally blood is going to go from the high pressure system and to the low pressure system so it'll go from the left ventricle into the right ventricle what that will do is that will cause the patient to present with a murmur so usually they're present with a murmur some type of holocystolic murmur so if you hear a new murmur on the patient definitely one of these things that you want to think about and it'll precipitate heart failure generally it'll cause the patient to go into a right heart failure before they go into left heart failure so it's more common that they'll get right greater than left because think about it you're overloading the right ventricle blood is squirting from the left ventricle into the right ventricle and you're overloading the right ventricle so that's something to think about but in a patient who presents with hemodynamic collapse in a hole of systolic murmur think about a vsd the other one that's also really interesting as well that you really want to think about here is going to be a patient who presents with what's called a papillary muscle rupture so let's say that they have an occlusion here and this occlusion what it does is it knocks out the blood flow particularly this you can you can see with a bunch of different types you can see this usually with inferior ischemia so usually right ventricular or RCA occlusion so if a patient develops like an RCA occlusion what can happen is this can cause a papillary muscle ischemia so this will cause papillary muscle ischemia or infarct let's actually let's say infant so again you have an occlusion there you're infarcting the tissue that's in stemming and stemi you develop an infarct of the papillary muscle when you infarct that tissue now it's supposed to be holding onto the chordae tendine it can't hold on to the chord A10 anymore and so if you can't hold on to this chordatanine what is it going to do this sucker is going to break right off it was supposed to be anchoring it down now look at it's flapping in the Wind because of that you can't hold this valve down and what happens is this valve becomes super unstable and it can easily whenever the patient goes into like statistically whenever they have what's called ventricular systole this valve can blow right open and now you get something called regurgitation now a regurgitant jet instead of going this way can fly back into the left atrium and so you really want to watch out for that so when a patient develops on RCA occlusion they infarct their papillary muscle what happens is they can develop what's called acute mitral regurgitation and that will cause a murmur Believe It or Not similar to a vsd a hollow systolic murmur and we'll put the patient in two heart failure usually in this particular scenario left more than right obviously because it's going to be affecting the left side now so these are the things that you really want to watch out for pretty scary one again not as common in the reperfusion era this last one is probably the most terrifying this one I feel like most people usually just die because they go into PE arrests because they're left ventricle just explodes but what happens is you get a really big LED occlusion usually in combination with the left circumflex but what happens is you infarct this entire left ventricular free wall imagine this whole thing is dead super weak as it becomes weak boom this entire free wall ruptures oh my gosh this is so terrifying blood that's in your left ventricle will then squirt out right into your pericardium as the Blood starts filling into the pericardium what is this called hemopericardium imagine all that pressure from here left ventricle just squirting blood into that pericardium that is terrifying so what happens is you get an LED occlusion you get a free wall infarct this thing causes a free wall rupture and this will push a patient into what's called what is this when you have a lot of blood that's accumulating within the pericardium and it's squeezing on the heart not allowing for it to properly fill it's called cardiac tamponade so this is another one that you want to watch out for we'll talk about this in the pericardial disease section but you want to watch out for a patient developing that Bex Triad right so the jugular venous extension the hypotension and the muffled heart sounds that would be another really really big one and then again you can potentially see signs of like pulses paradoxes but again we'll go over all that in the pericardial disease section all right this is another potential complication the last one that I want you guys to watch out for here is again another type of LED occlusion so if you get an LED occlusion and then what happens is it infarcts this particular tissue here right so you could develop some depth of this tissue then what happens is something kind of weird it ruptures but it doesn't rupture the way that you would normally think so it doesn't completely rupture the free wall and what happens is you develop a rupture here but it's kind of contained there's like a fibrin kind of like clot that's kind of stabilizing the rupture so it doesn't allow blood to empty into the actual pericardial cavity so it's a contained rupture we don't call this an aneurysm per se even though it kind of looks like it it's a pseudoane or a contained rupture so we call this it creates a pseudo aneurysm the problem with this is that now blood can kind of just stay in this area this can create like a stasis of blood flow what happens when you create stasis of blood flow clots Virgos Triad right and so then this can lead to clots forming here and if you get a clot that forms right in here and then it decides to flick a part of that clot off what do you get thrombo and bottle complications that patient gets like a stroke or something right so you want to watch out for thrombo and belai these are the big big things that I want you guys to associate in patients who have had an end stemi or a stemi all right now that we've covered all the pathophys the issues and the complications of myocardial ischemia and coronary artery disease now we're going to do is we're going to learn how to diagnose these diseases a patient comes in they have anginal chest pain and the classic way that I taught you guys what do we do first thing EKG you can add on some cardiac biomarkers like troponin and ckmb but they're not always going to be the first test of choice ECG should be the first test once you've done that if you see this it's normal there's nothing really bad about this you can get a troponin if it's negative that again supports the concept that maybe this is a stress induced ischemy and we didn't stress them enough so maybe this is stable angina we'll talk about the workup of that in a little bit if you have a patient who doesn't have stress induced angina then you're thinking that they have an acute coronary syndrome that this doesn't require change in demand so that's going to be things like T wave inversions ST segment depressions and then you're thinking about things like an N stami or an unstable angina how do I determine that I want to know which one developed an infarct that's the importance of the pathophysiology if it's ischemia they'll have a negative troponin that's unstable Angela if the troponin is positive that means that they had an infarct that's an nstemi if I see this so that's a stemi right there right that's a big old Tombstone thing you know things are puckering up down there that's not good this is St elevation this should make you think about a stemi if you checked at your opponent and it's positive it would be way more suggestive of an SD segment elevation of mine there is this potential though that if you see St elevation and a patient known as cocaine tripped hand smoking younger respond to calcium channel blockers and their troponin is negative it's a little bit more suggestive of vasospastic angina all right that's how I would start this process chest pain EKG cardiac biomarkers determine if the patient has the worst case scenario which is a stemi if they have a stemming what do I do I want to know where the heck that stem is so then I'm going to try to localize the stemi and this is where EKGs are going to be a little bit more helpful in your exam so what they'll do is they'll say hey here's an EKG what do you think is the vessel that's occluded so the first one here is going to be an anterior and I told you that's V1 to V4 I look for any St elevation in these leads and if you see that that would be suggested that the LED may be occluded if you're looking at the next one which is an inferior one you're looking at two 3 in avf and I see SD elevations maybe the right coronary artery is occluded with that being said if you think are right if you have an inferior Mi you should always do right-sided chest leaves just as a quick aside because it may show that the right ventricle is actually becoming infarcted and that's important to be able to identify but nonetheless lateral the left circumflex it's one and then AVL and then V5 and V6 you're looking for St elevations there and that would suggest the left circumflex is occluded and then lastly if I see St depressions or T wave inversions in B1 to V3 I slap on the posterior chest leads in V7 to v9 and I see SD elevations that's suggestive of a PDA occlusion this is the way that they could try to test you on the exam as to where the actual stemi you think is occurring which vessel is diseased or occluded now with that being said ECGs are really really good combining it with an echocardiogram is even better because what you're doing is you're kind of making a correlation between the chest leads where you think the vessel is actually occluded and then correlating that with wall motion abnormalities where the areas of the ventricles aren't Contracting very well with the vascular territory so you can kind of see here I'm not going to go crazy because you won't be heavily tested on this but if you see V1 to V4 St elevations and you look on the Echo and you see that the this territory the LED isn't Contracting well then you can say oh man I really think that this person is having a stemi and this kind of correlates and you can even correlate this with nstemi's as well but that's an important thing to do is to correlate hey anterior wall motion on rally hey maybe the LEDs knocked out RV is not Contracting very well they have an inferior wall motion abnormality maybe the RCA is knocked out left circumflex knocked out oh maybe that lateral wall isn't really Contracting very well or maybe the posterior walls are Contracting very well correlate your Echo with your ECG all right lastly in most patients on your clinical vignette you're going to get the ECG you're going to see that they have SD segment elevation maybe you get a troponin that's positive they're having crushing chest pain what's the test of choice but it's also the therapeutic like option in these patients it's usually going to get a coronary angiogram the benefit of this is that you're going to be for most patients when they get in the angiogram you're showing the occlusion but you're also going to treat the occlusion you're going to go in and put a stent in that area you're going to balloon it open and put in a stent but this is a really good test and probably the best test to find where the occlusion is so again you'll snake a catheter up there shoot contrast and look to see which of the vessels are not filling and where is the occlusion and again that's one of the best possible tests you could do all right so if a patient has a stemi go through that progression what's the ECG show where would a potentially localized correlated with your Echo and send them to the actual cath lab to find the occlusion and then treat the occlusion if they present with a normal ECG and a normal troponin then we're thinking about that stable angina patient but we still are scared because they have anginal chest pain we would want to send them for a stress test so we've ruled out ACS and we're going to say can the patient exercise if they can then you want to go ahead and do what's called stress exercise testing and so what we'll do is we'll kind of say okay there's a couple different options we could do here we can get a baseline ECG or we can do what's called a myocardial perfusion imaging where we give them like a radioactive tracer that shows areas of perfusion in their heart or we can do an echocardiogram and see if it's squeezing normally once we do that we're going to make them work out get them on a treadmill and have them Reach the kind of a target heart rate once we've done that and they start to experience maybe any symptoms or they get tachy arrhythmias or we actually repeat the ECG MPI or echocardiogram what are we looking for after we've really stressed the heart if I see on the ECG oh there are signs of ischemia that's stress-induced ischemia that would be helpful in telling me that this is a positive stress test if I didn't do the ECG test and I did the MPI then I'd be looking for areas of poor perfusion if I have to make them work out and I increase their demand now these errors are going to becoming suffering they're going to suffer now and the last thing if I do an echocardiogram and I see areas that aren't Contracting very well maybe they have an lad really big plaque there and I see that their anterior wall isn't Contracting very well after I had them exercise I could say oh there we go we have stress to induced wall motion abnormalities so these are all ways that if this happens and we see these changes that's a positive test now the reasons why you would do an NPR an echocardiogram because usually this is the first line is if their ECG has some weird things on them usually if they have like a left bundle it makes it really hard or if they have Q waves it makes a little bit difficult so you may do an echo or an MPI in those scenarios okay but we go to the other end of this algorithm which is the patient cannot exercise maybe they have terrible osteoarthritis they have some type of like rheumatological condition where they can't ambulate they just they can't do these things they can't exercise at all in those scenarios then you have to kind of precipitate the same increase in demand by giving them drugs two of the things that we would do is we would again get a baseline MPI or an echocardiogram and then we would give them a medication that would either really reduce the supply or increase their demand one is adenosine or dipridamole and what it does it decrease the supply it's actually really cool I'll show you how it does it in a second but I'm going to get the Baseline see what it looks like and then give them this drug and what it should do is if they have stress induced ischemia it should produce cold spots on their MPI I could also do the same concept give them an echo look for any like contractions of their ventricles give them dobutamine that should make their heart have to pump faster and pump harder which will increase the demand and it should show wall motion abnormalities and that would be a potential stress-induced ischemia now let's explain this adenosine or dipyridamole it's actually really cool it's called coronary steel syndrome here we give diaperinol or adenosine what it does is it does not vasodilate the disease vessel and it dilates the normal healthy vessels if you dilute a vessel you reduce the systemic vascular resistance and you drop the pressure in this area and it's easier for blood to flow in this direction but then what happens is you don't dilate this vessel the pressure doesn't drop in this area and now blood won't want to go this way it'll want to go to the lower pressure circuit and so this is literally going to steal blood away from the diseased area the supply is already reduced you're going to reduce it even more and that's going to precipitate ischemia and cause poor areas of perfusion so that's the concept of this pretty interesting either way you do any of these tests and it becomes positive usually the next thing is to say okay let's try to treat the patient we know that they have some type of stress this ischemia let's try to get them a little bit better but if we have any inkling that this patient may need to kind of go and get revascularized do something like a coronary angiogram look for the actual occlusion determine the severity of it or coronary CTA it's non-invasive and this will help you to determine to look at the actual vascular lesion so here's a coronary CTA and then here is a coronary angiogram to look for any kind of lesions that are present so you can see here's like this little stenotic area and you can see kind of stenotic areas here as well but that's the concept now after we've done this we've now determined the approach for stable Cad and the approach for stemi the approach for patients who have nstemi and unstable angina you really kind of just determine them already you determine if it's unstable angina or nstemi based upon the troponin and you're going to treat those guys relatively the same now that we've done this how do we go about treating the first patient which is the stable patient well the first thing is you don't want that plaque to rupture but more importantly if that plaque does rupture I don't want to thrombus to form on the plaque because it'll become subtotally or totally occluded and then I end up with an ACS scenario so how do I do that aspirin simple next thing is I really want to reduce their anginal chest pain so I want to reduce the oxygen demand so the ways that I can do this nitroglycerin because that reduces preload and dilates the coronary vessels and the second thing which is even more beneficial than that is beta blockers there is other drugs so there's not just nitroglycerin this is short acting but the drugs that you can give for long acting effect would be things like isosorbide dinitrate and there is the benefit of calcium channel blockers as well so it's usually beta blockers then PRN sublingual nitroglycerin long-acting isosorbidden nitrate which is another type of nitro and last line is usually calcium channel blockers and then after that there's another one called renolazine but we're not going to go there all right you've treated the patient with Aspirin you put them on a beta blocker they have sublingual Nitro you've treated them with isosorbent nitrate but now the patient has a positive stress test that is really really bad they have an angiogram which they got and it showed really really bad lesions like an lad that was like super stonotic or they have been symptomatic despite aspirin despite statins despite a beta blocker isosorbent to nitrate sublingual Nitro Etc and they're still having chest pain these patients have to be revascularized so when you want to revascularize these there's two options there's PCI or cabbage how do I determine if there's no left main lesion no left main coronary artery lesion they have less than three vessels that are plaqued up and they have a normal left ventricular EF it is preferable to do a PCI so a percutaneous coronary intervention now what we do is is we open up the artery we take a balloon we inflate the balloon and they're going to kind of try to open up and expand this area then what you're going to do is is you're going to pull back the balloon and leave in this stent which is going to hopefully keep this vessel nice and open that is the concept here but once we place this stent in we do not want the stent to clod off and we'll talk about what we'll do for that in a second what about the patient who gets the Cabbage it's the exact opposite they got a left main coronary artery lesion they got three or more vessels that are plaqued up and they're EF stinks probably better for these patients to get a cabbage a coronary artery bypass graph so they have a lesion like right here I'll take a graft and I'll move this over this way and sometimes we'll take like the internal mammary artery or we'll take the greater saphenous vein and we'll take those veins cut pieces of them and use them as the graphs to bypass these lesions you see how we're bypassing all of these lesions here that's the concept but to come back here we put the stent in when I put a stent in I don't want it to throw on bows and so I'll put them on Dual anti-platelets so in other words they'll be on aspirin plus something like Clopidogrel or decagitalor for at least one year then after that year you can downgrade to just one of those anti-platelets whether it's aspirin or it's Clopidogrel but I have to keep this on so that they don't stent uh thrombos this stent because that's terrible they can develop a reinfarction so that's the concept here here is the actual kind of like stent here and I want to prevent this I do not want them just like completely thrombos that stent all right 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 isosorbet and nitrate for long-term control beta blockers if need be add on the Statin they're still symptomatic angiogram shells high risk lesions the stress test is really bad revascularize them PCI based upon this cabbage based upon this if they get the stent they need do anti-platelet therapy for a year all right unstable angina and nstemi it's similar you first want to prevent the thrombus from propagating so you give them aspirin plus Clopidogrel plus Heparin that's the big difference you see how the we load them with this before we even revascularize them so we load them with Aspirin plus Clopidogrel plus Heparin so it's called dual anti-platelet therapy plus heparin now if I want to revascularize the patient with unstable angina or an ends to me I need to have particular indications and there's usually three one as I do what's called a wrist stratification tool called the temi score there is other ones out there this is the one that sometimes is tested on this step too if the Timmy score is greater than three that in that kind of predicts a higher mortality rate for these patients and that means that they should probably go to the cath lab and get revascularized the next one is if they develop cardiogenic shock remember I told you the two big complications of Mis is vtac vfib because you can cause a ventricular arrhythmia or cardiogenic shock from a really nasty infarction 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 and the last one here is refractory angina they're symptomatic despite aspirin dual antibody therapy Heparin they're symptomatic despite beta blockers Nitro morphine statins all of those things they need to get revascularized and the decision of which revascularization technique is the same and then if you stent them you need dual anti-plated therapy for at least one year okay we come to stemi if a patient has a stemi it is the exact same process you load them up you give them 325 of aspirin you load them up with Clopidogrel or take Agra you load them up with Heparin and put them on a Heparin infusion and they go to the cath lab as soon as they possibly can and again most of the time you're going to be placing a stent and these rare scenarios you may be considering a cabbage but most of the time you're going to be going to the cath lab what if the patient is at a hospital that does not have a PCI capable facility then you give them the TPA and you transport them as quickly as you possibly can to a PCI cable facility to put a stent in no matter what even if they get TPA the guidelines say that they should still get PCI done that is the concept here all right the last thing that I want to add on here is after the patient has received revascularization you want to prevent ventricular remodeling because this has been shown to be beneficial if the patient is hypertensive or their blood pressure can tolerate it you want to get them on ACE inhibitors or arbs because it's been shown to reduce the ventricular Remodeling and that is the treatment for stemming and that my friends covers coronary artery disease I hope you guys liked it hope it made sense and I hope it helped as always until next time [Music] foreign [Music]

Channel: Ninja Nerd

Views: 78,052

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

Id: 67tUtS3y_GA

Length: 52min 22sec (3142 seconds)

Published: Mon Mar 11 2024