hi everyone Dr Mike here in this video we're taking a look at es schic heart disease we're also going to focus on acute coronary syndromes like angina and myocardial infarction Mi which we call a heart attack and the associated ECG changes let's take a [Music] look so to begin we need to Define what a schemi heartart disease is first thing about es schic heart disease is it's the biggest killer worldwide so over 30% of Americans over the age of 35 will die of es schemi heart disease so it's really important we understand the pathophysiology of this disorder now heart disease makes sense it's a problem associated with the heart but let's define esema when I asked my students what is es schia I get a number of different answers which are all correct at least in part and one of those answers is a drop in oxygen supply so when I ask my students what is aeia some of the answers is a Dro in oxygen that's true which we call hypoxia but that's not only esia esia is in addition to a drop in oxygen it's also a drop in nutrient delivery and it's also a drop in waste removal and the reason why this is the case is because esia overall is a reduction in blood flow and this is really important because if it was just hypoxia just a drop in oxygen yes there would be problems but we wouldn't get the significant problems we see in es schia there are conditions where we have low blood oxygen like anemia for example and cyanotic heart disease but we don't get the same effects as we do in es schic heart disease and it's because it's compounded by the fact that it's not just a drop in oxygen but also a drop in nutrient delivery and also a drop in waste removal from that area so esea is an issue with blood flow a decrease in blood flow to the heart muscle itself decrease in this case esic heart disease decrease blood flow to The myocardium and The myocardium is the heart muscle now we need to have a think about the blood vessels that feed the heart itself which we call the coronary arteries so I'm going to draw up some of the coronary Aries cuz we're going to go back to it because it's very important so let's draw up here a heart yeah that's not too bad there's the Apex which is the pointy bottom there's the base strangely which is the top and we're going to draw up the arteries that Feed The myocardium so the arteries that are going to be affected here firstly we've got the aod the aod is going to leave the heart now at the base of the aod we're going to have two little outflows one's going to provide us with the left coronary artery and the other one's going to provide us with the right coronary artery so we're starting here left right now let's take a look the left coronary artery what you're going to find will Branch pretty much straight away so it has a branch that comes off like this and that Branch moves behind the heart as well like that I'll talk about what that's called in a sec it also has a branch that goes down towards the apex of the heart now with the right coronary artery the right actually moves its way all towards the right hand side of the heart and begins to spin its way around the back but it also can have a branch that moves down the back of the heart towards the Apex as well so what we've got here now there's many and there's other branches that come off these but these three to four you really need to understand when it comes to acute coronary syndromes particularly M hard attacks so what are the names of these branches so we're going to have what we call the left circumflex right lcx left circumflex we're going to have the left anterior descending sometimes known as the anterior interventricular artery great name we're going to have the right coronary artery which includes this around the back here and we're going to add the posterior descending artery here so this is important because you can just look at this and go oh I can sort of see where these blood vessels feed now these coronary arteries are epicardial so remember if we have a look at that and this is going to be important later as well everything's going to be important for later if I have a bit of Heart Like That crosssection of a heart and I've got the coronary here you can see it's sitting upon the outside of the heart so let's say here's a layer of the outside of the heart here's the thick inside layer and then here's the most internal layer which is lining the inside of the chambers of the heart so this is going to be epicardium this is going to be myocardium and this is going to be endocardium and here is a blood vessel a coronary artery that you can see they are epicardial the coronary at least the first couple of centimeters of them and then they start to embed themselves and become intram cardium all right now important thing is in es schic heart disease most of the coronary arteries are affected at the epicardial portion the ones that sort of sit on the outside all right so we've got these four you must know let's draw this in a different way let's do a bird's eye view of this and let's take the heart I'll draw it like this this bird's eye view of the heart and let's have the right and left right ventricle left ventricle we've sliced we've done a transverse section we looking bird's eye view down into the heart and we're going to draw up these four coronary arteries 1 2 3 four let's name them we've got the left circumflex we've got the posterior descending artery we've got the right coronary artery and we've got the left anterior descending sometimes known as the anterior interventricular artery let's have a look this is all my cardium right this is all the thick muscular tissue of the heart let's see where it feeds let's start with the lad let's color the tissue that it feeds in purple the lad is going to feed 2/3 of this interventricular septum and most of the anterior wall of the left ventricle so basically left uh sorry the 2/3 of the septum and the anterior wall of the left ventricle all right let's take a look at the left circumflex this one Fe feeds the lateral wall of the left ventricle let's have a look at the right coronary artery now the right coronary artery will feed all of the right ventricular wall and also it will feed about 1ir of the posterior wall of the septum as well and because remember the PDA is a branch of the right coronary so sometimes you can talk about them together you could say that the PD with the right coronary artery will also feed the posterior inferior wall of the left ventricle now remember this is a bird's view of the top we can't see what's happening further down but we can see that the right coronary with the PDA will feed the posterior inferior wall the back and down the bottom all right so now we can see where these arteries feed this is super important because in es schic heart disease we've got reduced blood flow of these arteries now the question is what is reducing the blood flow of these arteries all right let's take a look let's draw up the main causes of esia now there's one which is by far going to be the biggest cause of aeia and that's what we call atherosclerosis so let's write down athero sclerosis now we've done a video on atherosclerosis these are lipid based or cholesterol based plaques that can form under the uh lining of the blood vessel which we call the endothelium so think about the blood vessel just as a quick recap you got a blood vessel here and you've got epithelia remember one of the four tissues of the body epithelia connective nervous and muscle you've got epithelia lining the inside surface smooth flat cells that allow for the blood to move through smoothly perfect in AOS osis you actually get a buildup of fat underneath these so remember the blood vessels going to have multiple layers right so underneath here you get a buildup of plaque fatty tissue that occurs and it forms this plaque and you can still have the epithelia sitting on top of that plaque right so that's an atherosclerotic plaque right here so atherosclerosis is number one more than 90% of es schic heart disease is caused by atherosclerosis now if we take a look at atherosclerosis there's two major types of atherosclerosis that can occur so you can have the plaque that forms so if we draw the blood vessel like this and we draw a plaque like that you can see that it's blocking part of the hollow Lumen the hollow inside so that's just the hollow pipe of the blood vessel we're looking through it like we're looking down a pipe and you can see that you've got this plaque that's built up now there's a type of atherosclerosis where the plaque has a cap on top of it and it's what we call a stable plaque it's stable meaning there's no indication that in the short term at least it's going to rupture or get worse in at least in the short term the acute phase so it's stable now what this means is think about it this is one of these arteries feeding the muscle now at rest that might be enough space for blood to get through to feed The myocardium at rest but as soon as you increase the heart muscles demand for oxygen now what can you do to increase the heart muscles demand for oxygen if you increase its heart rate or you Inc increase its contractility right so anything that increases its cardiac output the amount of blood it squirts out every minute that's going to increase its demand for oxygen nutrients now the thing is generally speaking blood vessels can do this because they can relax and dilate and get bigger but in this case it's not going to help very much because it's still blocked and if there's a blockage and it's the supply of oxygen and nutrients do not meet the demand so here the de demand goes up but the supply has gone down so it doesn't match right it's not a nice ratio this results in esia and this is what we call a stable plaque esia and the esic event that we get is result results in something called angina which is chest pain so this can result in what we call stable angina I'll write esia first because it is eske an schic event occurs es schia and this esia results in stable angina now angina as a term sometimes you'll see it written as angina pectoris that literally just means chest pain right so aeia resulting in chest pain the tissue is not getting oxygen nutrients the heart freaks out and sends signals via the nerves going uh I'm in pain so you get chest pain but you can also get jaw pain and it can radiate down the left hand side of your arm which we call referred pain so this is angina pectoris that chest pain now in this case for stable angina what's going to increase the heart rate contractility in cardiac put anything that increases exercise so think about exercise or sympathetic nervous system stimulation so what could do this exercise that makes sense your heart rate goes up but what else can increase heart rate contractility and cardiac output sympathetic nervous system your phlight system now what stimulates your sympathetic nervous system well yes exercise but also stress and anxiety and it doesn't just have to be uh physical stress it can be emotional stress so some people can get stable angina from emotional stress and that's important because the demand goes up the blood can't feed the tissue the tissue starts to become es schic it's not dying it's not dying it's just becoming es schic and you get the chest pain now in stable angina because that plaque's not getting worse at least in the short term if you stop the exercise and and reduce that stress it should resolve and so it should all resolve within 20 minutes 15 to 20 minutes also if you gave them something that vasodilates opens that blood vessel up like nitrates then that should resolve it as well so in stable angina it should resolve once you stop the exercise stop the emotional stress or physical stress and give somebody nitrates something that can dilate the blood vessel or even calcium channel blockers all right that's stable the other type of atherosclerosis is probably unsurprisingly the unstable now in the unstable we've still got that plaque but it doesn't have that nice cap on it so something has disrupted that plaque and the disrupted cap and top of the plaque will expose the lipid insides to the blood that's moving through now remember you've got platelets inside that blood that's moving through and platelets are very sticky they have to bind to anything that's presenting themselves so in this case in unstable I'll write that first in unstable you'll have platelets accumulating binding two and accumulating and platelets due to positive feedback start to one platelet will recruit another which will recruit another and another and it starts to form what we call a thrombus a thrombus which is like a blood clot now as you can see this thrombus can start to olude or block The Vessel now this is going to be an acute short term because this happens really quick right so it bursts it exposes itself platelets come in starts to block block block and it starts to olude or block that vessel quickly and it's unstable now this quick change results in something called an acute coronary syndrome so unstable can result in an acute coronary syndrome and an acute coronary syndrome is unstable angina and Mi myocardial infarction so this is death now in unstable angina it's similar to this in the sense that it's just chest pain due to an unstable plaque now if it lasts too long it can progress into a myocardial infarction because the infar in this case is telling you that tissue is now dying so here for stable angina here for unstable angina there's no death of the tissue and that's important because if somebody comes in to present in the Ed in the emergency department and they've got chest pain and you're sitting there thinking what could be the cause of this chest pain you go through all your differential diagnosis you go it could be reflux it could be uh trauma it could be muscular sceletal it could be what whatever you go through if you take Bloods and you have a look at certain levels of proteins that would get released during cell death myocardial cell death things like troponin should be relatively negative for these two because there's no cell death but if it progresses to Mi cell death you'll see troponin now the acute coronary syndrome is short term no cell death cell death now I'm going to talk about mi in a sec because we're going to focus on it but the unstable angina the difference here in in addition to the thrombus that's formed is that uh it may not be induced by exercise or the sympathetic nervous system it may not resolve if you stop those things either that's important it can last longer than stable angina and it may or may not be benefited by Vasa dilators now if we have a look so this is 90% of the causes of schic heart disease let's have a look at a couple of other causes so you've also got vasospasm that's another cause of es schic heart disease now vasospasm is interesting vasospasm is when you got your blood vessel and it spasms and constricts so there's two major types of vasospasm so let's draw the blood vessel and then it's constricting like that and with can call this a transient vasospasm so it's just happening short term and you can have a more longer term vasospasm so this is going to be a longer term or more severe vasospasm uh longterm all right now what's the difference here this transient vasospasm will result in chest pain so angina which we call Prince metal Prince metal angina so again it's just saying it's it's chest pain but it's chest pain caused by a transient constriction which means it should be fixed with the nitrates with the vasodilators so three major types of angina right stable angina unstable anina and prin metal angina the severe longer term vasospasm well this can cause an MI because it will constrict for such a long period of time that it doesn't deliver the oxygen nutrients and waste and therefore the tissue starts to die and have an infact all right the last cause or there's a couple of others but the other major cause is going to be uh microvascular dysfunction microvascular dysfunction what we've spoken about so far are the macr vascular the big blood vessels right the coronary arteries but in this case we're talking microvascular so the capillary beds or the at least the smaller blood vessels now in this case you can have quite severe so in you can let's just have the blood vessel here's the bed the vascular bed or at least the capillary bed and you can have some damage that occurs to it so let's just say you know a minor relatively minor damage what this can result is it works can work on a background of these things so it can contribute it can contribute to acute coronary syndrome acute Ute coronary syndrome now the other one is a more severe microvascular damage and this severe microvascular damage can actually result in tsubo myopathy have you heard of teasu myopathy teub myopathy is broken hearts syndrome or Broken Heart disease sometimes called stress induced myopathy you ever heard of somebody their loved one has died and they died of a broken heart this is what they're referring to te a sub myopathy it can be due to a severe issue with the microvascular bed being damaged we don't know how this is happening but it can be a whole bunch of pro-inflammatory events occurring resulting in the smaller blood vessels dying off and it damages the left ventricle ability to contract properly so as you can see with schic heart disease is atherosclerosis is the major cause and then you've got all these others I want to focus on Mi because I want to talk about how when we've got damage to the blood vessel and we not only get aeia but death of the tissue how we can pick this up on an ECG so let's take a look so when we talk about Mis myocardial inunction there's two major types right you can have what we call a an n stemi and you can have what we call a stemi now interestingly they're named after what you see on an ECG so n stemi is non St elevated myocardial infarction and a stemi is an st elevated Mardin function so let's think back on an ACG what do we see on an ECG we can see a normal ACG let's draw it in the middle p q r s and t so we got the P wve the Q the r the S and the t-wave on the ECG now this is what you generally see when you're looking at lead 2 on the ECG now let's just recap quickly of the different leads of an ECG here we've got the heart sitting within the chest you can put chest leads on you can put limb leads on they give you views of the heart from an anterior posterior View and the limb leads give you a view of the heart from Superior inferior point of view as well so if we were to just have a look at the precordial or chest leads and draw them up they're going to go around the heart like this and you're going to have V1 V2 V3 V4 V5 and V6 they're the chest leads and they're looking at the heart from front to back that's the perspective they have of the heart then you've got the limb leads and these limb leads will look at the heart you've got AV L AVR AV VF lead one lead two and Lead three remember they're looking at the heart from this perspective right from this angle this is where they're looking at the heart all right so in this particular lead Trace here that we get that's from lead two so it's looking at the events happening in this direction of that lead either towards or away from lead two now the interesting thing is with an N stemi what we get is a non St elevation and you can actually get what looks like an ST depression so you get a p q r s t like that so what we see is the ST segment is depressed and when we have a look at stemi what we get is a p uh uh sorry p q r s t and you get the St elevation how interesting why what's the difference outside of the ECG when we look at an n stemi and draw the heart up itself if this is going to be the heart for an N stemi there's the right Atrium left atrium right ventricle left ventricle and in stemi the death remember you're getting esema and then death of the tissue it's happening it doesn't have to be this particular position but what you can see doesn't go the full width of the heart muscle itself it's goes from the sub it goes from the endocardium the subendocardium so this is called subendocardial endocardial esea or infar to be more specific in this case so it's a subendocardial esia leading to infar but let's just write subendocardial infar as you can see sub endoc cardio but let's draw it up here for this one for the for the stemi same thing right atrium left atrium right ventricle left ventricle for a stemi it goes the full width of the tissue the infar so it's not subendocardial it's it goes through the whole wall and the term we use for that is transmural transmural infar oreia now because of these differences is the reason why we either get St elevation or depression now before we go into the specifics of that what we can do is if you get an ECG Trace right you get how many lead leads do you get on the ECG 1 2 3 4 5 6 7 8 9 10 11 12 12 lead ECG 12 different views of the heart and because we've drawn it up like this we can actually go okay I'm seeing an st elevation in not all the leads but some of the leads where is the death of the tissue happening is it happening there is it happening there is it happening there is it happening down here where is it happening you can look at that through the ECG so as you can see here if you get death of the tissue sorry if you get in an ECG trace an st elevation in V1 2 3 and 4 well you can see V1 2 3 and 4 is looking at the septum or the anterior wall of the heart so if you see St elevation now I got to find a place to put this let's say you see St elevation in V1 to V4 that tells you that there is some es schic event of the septum or anterior wall of the heart and we know that what is the vessel that feeds this part of the heart the septum and anterior wall it's the lad so you can see that oh it's likely going to be a problem with an occlusion or blockage of the lad okay let's have a look what if you were to see something in v56 and Lead AVL and one so let's say we saw something in V5 V6 AVL and Lead one hm V5 V6 AV lm1 well it's telling me it's the lateral wall of the heart and we know that the lateral wall is fed by the left circumflex so that's telling me that it's a lateral wall in fact so the death is happening in the lateral wall left lateral wall and it's probably going to be the left circumflex all right what happens if we see St elevation in leads three avf and two leads three avf and two well that's telling us that it's the inferior wall of the heart so the inferior wall and we know that the inferior wall of the heart is going to be the right coronary artery and PDA so we could say well it's the right coronary artery and or posterior descending artery so hopefully this helps you because whether it's an ST depression that you see in these leads or an elevation in these leads that's simply telling you it's either going to be subendocardial not the full width or transmural the full width and it can give you an indication as to not just where on the heart but what vessel might be uded that's really really helpful now just very quickly to talk about why it it is an st elevation or an ST depression on the lead it has to do with once you have a schema of these tissues the ions that make up the the the my cardum the cells itself they change in regards to where they're sitting inside or outside the cell so I'm just going to quickly draw it up here if you were to have the heart and you've got lead two looking at it from here and you can see lead two there right where it's looking looking at it from here that's our Trace lead that gives us that normally if you've got a sub indicat your death so this tissue is undergoing aeia first of all and then dying we know that inside of our mardial cells we've got heaps of potassium right but not much outside if that cell dies this potassium leaks out or even if it becomes a schic it leaks leaks out because there's ATP dependent channels that keep it in if the ATP is gone it opens up and potassium exits now when the potassium exits it changes the excitability of these cells and strangely it makes them more excitable and they depolarize which means that usually at rest when no electrical event is happening at the heart right this part here at rest when no electrical event is happening these cells are depolarizing early remember that's the first depolarization event of the Atria that's the second of the ventricles but if this is depolarizing early that flat line that we see which we call the isoelectric point right which is that if they depolarize early that moves up which means let's draw it up here right here's the normal isoelectric point right that will draw that ECG on but that's depolarizing early and you can see it's depolarizing early in the direction of the lead which means you get a bump up so this first isoelectric point doesn't happen down here the isol electric point is moved up so now the isoelectric point is here and so in this case with subendocardial infar you'll have a normal you'll have sorry you'll have a p q r right on this elevated isoelectric point but then you get a normal s t down here and then it will drift back up because it's depolarizing early again right what do we get ST depression so in the subendocardial infa because depolarizing depolarization is happening early in the direction of lead 2 in this case what we get is an ST depression but as you can see this is 0o molts this is where it should be so in actual fact it's not ST depression it's everything else elevation if you wanted to be more accurate so that's subendocardial infar okay what's happening if you've got transmural so it's going the full length of the tissue well think about it the potassium is exiting and it's depolarizing these cells early but it's depolarizing them away from the lead early so let's draw it over here here's the normal isoelectric point right 0 molts but because it's happening depolarization is happening early away from the lead our isol eletric point is lower so now we've got our p q and then as we get our R then we get as you can see here right it goes up pqr [Music] S so we get an and then it drops back down to normal again so we get an st elevation in transmural so hopefully this is helpful we could talk about this all day but this is es schic heart disease also known particularly when it comes to unstable andina myad inunction acute coronary syndrome and some of the ways that you can make sense of it with ECGs and I'm Dr Mike thank you hi everyone Dr Mike here if you enjoyed this video please hit like And subscribe we've got hundreds of others just like this if you want to contact us please do so on social media we are on Instagram Twitter and Tik Tok at Dr Mike todorovich drmi k e t o d o r o v i c speak to you soon