ST Elevation and ST Depression EXPLAINED

hi everybody dr. Mikey in this video I'm going to show you why some types of myocardial infarction can demonstrate with an ST elevation or an ST depression in an ECG so first thing we need to do is we need to have a look at what happens in a normal heart muscle cell alright so remember that if I were to just draw up a heart muscle cell called a cardiomyocyte that if we would have a look at the ions associated with it sodium and potassium predominantly then you're going to have basically all of that sodium sitting outside the cell and all of that potassium sitting inside the cell and as we all know from basic biochemistry ions like to go down their concentration gradient so sodium wants to go down its concentration gradient go inside the cell potassium wants to go down its concentration gradient and go outside the cell all right the thing is that sodium can't go inside the cell because the channels for sodium are shut not letting sodium in potassium however does have channels that are open and so potassium can freely exit the cell of the heart muscle and that means potassium will leak out of the cell now I want you to think about this potassium has a positive charge with it and therefore carries that positive charge outside which means when we compare what's positive and what's more negative this positive stuff goes outside which makes it slightly more negative inside compared to outside in actual fact if we were to compare this charge difference the charge difference would be around about negative 90 millivolts now this is what is happening in a heart muscle cell when it's at rest when it's not contracting and this is what we call the resting membrane potential in actual fact if I were to draw up a graph here and have negative 90 millivolts here this is where everything begins so if I want to tell this heart muscle cell to contract what we need to do is we need to make the inside go from negative to positive and that's called depolarization and in order to depolarize this cell we need positive sodium to come in now you have certain stimuli that can tell sodium to come into the cell which makes it a little bit more positive it opens up sodium channels makes it a little bit more positive and it starts to drift up towards what we call a threshold which is around about negative 70 millivolts once it hits this particular threshold all the sodium channels open up all of the sodium moves into that cell it becomes really positive inside the cell and this is the depolarization event of the action potential once that's happened and it's hit its paint these sodium channels shut these potassium channels remain open and we open up some more channels which are calcium channels and we know that calcium going into the cell is what tells the muscle to contract so with that calcium going in no muscles contracting right now if you've got so remember these sodium channels are shut no positive stuff coming in from sodium we've got positive things going out which makes this go down slightly negative again but we've got positive calcium going in they basically balance each other out you hit a plateau alright then the calcium channels shut potassium keeps going out and then it goes back down and this is what happens the action potential for a heart muscle cell now I want to give you an example in which let's just say if we reset this back to resting membrane potential we've got the potassium leaking outside and we've got the sodium still outside and the charge is negative 90 we're down here alright so I'm gonna draw another one on this but let's just say something happens in which the concentration of potassium outside increases what that means is comparatively now the potassium there's still more potassium inside the cell but the concentration outside has increased its need to diffuse Outsiders reduced right if you've got a really steep grade in heaps of potassium here no potassium here it really wants to go outside if you increase the concentration out here potassium really doesn't want to go outside as much now what that means is potassium remains inside the cell and this is a little bit more positive than it was instead of being negative 90 it mightbe around negative 50 so let's now say let's have an example where for some reason we've got more potassium outside the heart muscle cell and it leads to the resting membrane potential no longer being negative 90 but being negative 50 what this means is is it's already began to depolarize which means this type of cell in this scenario has started to depolarize it depolarizes early and what happens is that if it starts at negative 50 sodium channels the fast-acting sodium channels don't work only that kept those calcium channels work and they're slow so it means the depolarization event the real sharp on that we've got here in red doesn't really happen it's quite slow and it finishes early and then repolarizes early what I'm saying is if I were to increase the potassium concentration outside of a cardio myocyte relative to the inside you get an earlier depolarization event and an earlier repolarization event keep that in mind because now we need to talk about what happens in St elevation and ST depression first thing is this a STEMI ST elevated myocardial infarction is where on an ECG trace which is the P wave QRS complex and T wave P Q s and T wave that st-segment is elevated and it looks a little bit I can get rid of this now it looks a little bit like this that's the st-elevation question is why does this occur now in other cases you can sometimes get an SP depression in which you have that that ST depression alright let's talk about how these scenarios occur first thing is this let's focus on the ST depression so that's the isoelectric point and that was the ice out that you're quite there and you can see ST elevation ST depression ah let's start with the ST depression in an ST depression it is representative of ischemia which means lack of oxygen nutrients going to a particular area that does not go through the entire width of the ventricle so let's just say we have an ischemic event happening here now I want you to think about this right what usually happens is if you have a lack of blood flow through the coronary arteries that feed the heart due to some sort of atherosclerosis or thrombus that is formed right it's first going to affect the sub endocardium which is this area here before it affects the rest of the tissue okay so the sub and akkadian first and this is this scenario where acting upon here is we're now affecting this area and what I've got drawn up on this side is zoomed in to that that's what we're zoomed in on which means we're now looking at this particular area here we've got this part of the tissue is not being fed properly let's make that a little bit bigger the point is the part that's not being fed properly does not go the entire width of a heart muscle you also need to know that obviously when we do an ECG there's going to be various electrodes and I'm sure you're watching this video because you know where those electrodes are placed we're going to have an electrode for example sitting here let's say that this is lead to for example so we've got lead to sitting here having a look seeing what's happening you know with ECGs that if depolarization happens in the direction of the lead right so if depolarization happens deep hole happens in the direction of the lead you get a bump up on an ECG if depolarization happens away from the lead you get a dip down if repolarization happens in the direction of the lead you get a dip down and if repolarization happens away from the lead you get a dip up this is the cheat sheet for ECGs as we all know all right this tissue is not being fed enough oxygen or enough nutrients what happens then is if there's not enough oxygen and nutrients your mitochondria can't produce enough ATP there is a certain type of potassium channel remember Tassie wants to go higher there's a certain type of channel that's blocked by ATP which means it remains shut when there's enough ATP present under ischemic scenarios no ATP those potassium channels open up and what will that result in so I'm going to draw a whole bunch of cardiomyocytes here right a whole bunch in this affected area all right not enough oxygen supply feeding this area not enough ATP what happens is the potassium channels open up and potassium leaks out of these cells that means what you now have is an accumulation of potassium outside the cell now I said to you what happens in scenarios if potassium increases outside the cell the potassium inside is less inclined to go out and it becomes more positive inside the cell which leads to early depolarization okay in tissue like this which has not fully become ischemic but in part Sabina cardian potassium increases outside the cell the potassium inside doesn't really want to go out so it becomes not negative 90 millivolts but more closer to negative 50 maybe and it depolarizes early now when is it depolarizing if we draw up the ECG right once you think about this there's different parts of an ECG let's just forget the P wave for the moment and we're starting here just before the QRS complex so you've got that then you're gonna have let's just start here if that's the polarized early in an isoelectric point when it's supposed to be right zero millivolts nothing's happening right what happens is this depolarization event it's happening early spreads out to the tissue that's not supposed to be doing anything yet it's the isoelectric point and it spreads out from this area when it's supposed to be just before the QRS complex when everything's supposed to be relaxing just before depolarization depolarization spreads in the direction of the lead and what that does is it raises up it raises up the isoelectric point because as you know if depolarization happens in the directional lead things go up you get a positive deflection and so what happens is zero millivolts we'll be around about here but we will start up here then as normal the rest of the ventricular have been ventricular myocardium depolarizes and this leads to the QRS complex right the QRS complex but once the whole ventricle is depolarized and then repolarizes again it doesn't care about this part that it missed and it goes back down to its normal region and what you have is an ST depression so in actual fact it's not the fact that the ST is depressed it's the fact that during the isoelectric point where nothing is supposed to be happening because of this ischemic event that didn't go through the entire width of the ventricular muscle it started higher and then after everything depolarized and repolarized it went down and therefore ST depression is representative of some and the sub endocardial ischemia not transmural or full degree full width ischemia now I want to talk about what happens if it's full distance let's now say that somebody is having an ischemic event it's blocked so much for such a long period of time that it goes the entire width it's called a transmural ischemia we can drop these cells and again no oxygen no ATP potassium channels open potassium leaks out of these cells and if potassium is high outside the cell all the other surrounding cells are less likely to diffuse potassium out and they depolarize but where can they depolarize they can only depolarize through this tissue and you can see this happens away from the lead which means at the isoelectric point in a transmural ischemia let's say that this is zero millivolts because it's moving away from the lead depolarization away the isoelectric point starts lower and then again you have the normal ECG P QRS and then what happens is normal depolarization for the rest of it normal repolarization goes back to the zero millivolt isoelectric point and now it looks like we have ST elevation but in actual fact what it was was at the isoelectric point before the QRS complex it began depressed therefore st elevation is representative of transmural ischemia so hopefully this helps you understand exactly what's going on in ST elevation and ST depression in myocardial infarction

Channel: Dr Matt & Dr Mike

Views: 267,911

Keywords: STEMI, st elevated myocardial infarction, st depression, why st elevation, why stemi, difference between st elevation and depression, NSTEMI

Id: vSrW4jg8Zq8

Length: 16min 8sec (968 seconds)

Published: Thu Mar 05 2020