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Welcome everybody. This is the uh first and my second series of talks. I gonna be talking about 12 lead E CG interpretation with a focus also of going on how to recognize acute infarction particularly. Should you be activating the Cath Lab? Is this acute coronary occlusion? But along the way, we will be emphasizing a systematic approach to E CG interpretation. So let's get started. The E CG in the figure was obtained from a previously healthy older man who contacted emergency medical services because of chest tightness that began one hour earlier. So given this history, how would you interpret the E CG? Should you activate the catheterization lab? And the question is, what would you do with this? So, yes, this patient is having a semi that's ST elevation, myocardial infarction. No, this patient is not having a stemi. So no, I would not activate the Cath Lab. Yes. Assume om I until proven otherwise. How many of you I'd love to know. I heard of the term om I occlusion based myocardial infarction. Prior to this talk, a couple of definitions, ST elevation, myocardial infarction. It's a millimeter based definition. ST elevation at the J point in two contiguous leads right next to each other. With the cut off point being at least a millimeter in all leads except for leads V two and V three. And the rationale for this is leads V two and V three often normally have a slight amount of ST segment elevation. So they need more and the criteria, this gets kind of complicated, doesn't it? If you're older than 40 years of age, then two millimeters is enough and leads V two and V three. If you're younger than 40 years of age and you're a man, you need 2.5 millimeters. If a woman, you need 1.5 millimeters. And I will tell you, I don't remember these criteria and I don't feel bad about not remembering them because I find they are not useful. It's based on the semi paradigm, which is an old and I believe fully outdated paradigm in 2023. But it's a paradigm that's still used. I still see loads of people including loads of cardiologists worldwide that are stuck in the semi paradigm. I wanna go over what's called the OM I manifesto. So om I is an abbreviation. It simply means an occlusion based myocardial infarction. It's based on the principle that with an acute M I most of the time, probably 90% or more of cases, there is acute occlusion blockage of a major coronary vessel and that's what causes the infarct if, if you're using millimeter based criteria stic criteria that I went over a moment ago, you're going to miss at least at least 25 to 30% of acute coronary occlusions. And if we think about what we're doing in acute M I, what do you wanna know what's the emergency? So you wanna know if there's an acute coronary occlusion because those are the patients who can benefit from opening up the acutely occluded vessel, whether you do this by thrombolytic therapy, depending upon what type of institution you have, what modalities are available or ideally, if you have access to cath lab that can be activated at any point in time. One of the key concepts regarding om I is to appreciate what happens with most infarctions, there's acute coronary occlusion and only the vessel closes. So what we wanna do is reperfusion. One of the things many people still do not appreciate is that spontaneous without any treatment at all, spontaneous reperfusion can occur when the vessel acutely occludes, the patient often gets symptoms. Usually chest pain. What do you think happens if the vessel spontaneously opens most of the time the chest pain will go away if the ST segments went up when the vessel was occluded. If the vessel opens, the chest pain will go away, the ST elevation will become less, it may go away. And as the vessel continues to reperfuse, you may get reperfusion, ST dash T waves usually in the form of T wave inversion. So that's the thought behind an O me. You can recognize an O ME. And this is the point that unfortunately all too many clinicians still don't recognize is the fact that they're still waiting for stemi. If you don't have a stemmy by those millimeter based criteria, they say we don't go to the Cath lab and that misses a window because by the time those patients get a stemmy, they're in trouble. Now, what happens if you had ST elevation? It lasted for maybe 30 minutes an hour, it goes away because there was spontaneous reperfusion. But the process may not be over because what spontaneously opened might just as easily spontaneously reclose. So if you have evidence that there was an only, even if there's spontaneously perfusion, the ST segment elevation is gone, the patient feels better that patient still needs reperfusion therapy ideally going to the Cholac to prevent spontaneous reclosure of the culprit vessel. These are a few things I won't have time to go into all of these today, hyperacute T waves. This is something you can recognize. Old computer algorithms do not recognize this newer computer algorithms by A I can potentially depending on the algorithm recognize it, but all of you can learn to recognize it. If you're not familiar with it, the T wave looks funny. It may have taller than expected peak, maybe fatter at its peak wider at its base. You can recognize this, this is based in proportion to the size of the R wave. And the lead, there is a magical relationship between lead three and opposite line lead. A VL. When you have an acute inferior infarction in the inferior leads of ST elevation. And most of the time you'll see reciprocal oppositely directed ST depression in a VL that tells you you have an OM I ST depression that's maximal and leads V two to V four. This oftentimes suggests an acute posterior om I. And the last thing here is dynamic ST dash T wave changes. It simply means that you started out with ST segments that were depressed or were elevated. The patient's chest pain either increases or decreases. You repeat the E CG. There's been a change. This is, it shows you the process is in flux, there was spontaneous reperfusion or spontaneous re occlusion. And if you see this, take the patient to the calf lab, let's get back to this tracing because one of my key goals for the series is to go over the systematic approach to 12 lead E CG interpretation. Those of you who attended my series on arrhythmias recall that I talked about watch your PS and Qs and the three Rs for my systematic approach to rhythm. Those are the five parameters to look for P waves, QR S with regularity of the rhythm rate of the rhythm. And if they're P waves that they're related to the QR S complex with 12 lead. Ec GS. We have another system, systematic interpretation does not, does not slow you down. On the contrary, it speeds you up. This is the most common thing that's overlooked, not having a system. So what is my system for 12 lead? So I wanna look at rate and rhythm. This is the same thing that we did with my first series. Watch your P's and Q's in the three RS. I next wanna look at intervals. There are three intervals, the pr interval, the QR S and the QT, the pr interval is long. If it's larger than a large box, the QR S is wide. If it's greater than half a large box, greater than 0.1. 0 and the Q TC, there are formulas for this, but in general should not be more than half the RR interval axis. I won't get into details today. Then we're gonna have chamber enlargement which we won't go into today. And then we have Q RST changes regardless of the system you use, whether you use my system or another system. If the QR S is why before you go further, find out why, why is the QR S? Why is it due to a bundle branch block or some type of conduction defect? And the reason for this is to save you time because if you have a bundle branch block, if you have WPW other conduction defect, then all of the criteria you're gonna use for axes for chamber enlargement and particularly for assessing for ischemia infarction will be different. So if the cures is wide, find out why it is wide. Before going further. Today, we wanna talk about looking for Q RST changes. I look at all of the leads, looking for the presence of Q waves, I look for R wave progression and then I look for ST segment and T wave changes. ECG interpretation has two steps. Step number one is the easy part I just described what I see rate, rhythm, intervals, axis hypertrophy. Q RST changes. Step two is the clinical impression. That's where we figure out based on the history what to do with the patient. So let's go back and apply this rate and rhythm that I can look at the to see an upright P wave constant pr interval. The rate is about four large boxes, 75. So this is a regular sinus rhythm. The rate is about 75 great rhythm intervals. The pr interval is not more than a large box. The QR S is not more than half a large box and I can look at all 12 leads for this cause. Sometimes part of the QR S may lie in the baseline but the QR S is narrow. It's a supraventricular sinus rhythm, no conduction defect. The Q TC I'm gonna look at the lead where I can probably see it the longest. It does not look to be significantly greater than half the RR interval. It's probably fine, right in the intervals, axis, I'm upright in lead one, I'm more upright in lead APF. So it's probably plus 60 plus 70 degrees or so. A normal axis chamber enlargement. Again, that's not the purpose of today. I'll just mention the number 35 as the most helpful number criteria, deepest wave and leave V one view all starwave V five V six. It's not more than 35 no chamber enlargement. We are up to Q RST changes. Are there any Q waves now lead. A VR doesn't really count for Q waves cause A VR is from the upper right quadrant that's looking away from the heart. But is there AQ wave in any other lead? What do you think? And how many of you recognize this really pretty big, pretty wide Q wave? It's especially large given the small size of the R wave. So that's AQ wave and looking at all the other leads, it's the only Q wave I see R wave progression. The R wave should get progressively taller and somewhere between V two to V four, the R wave should get taller than the S wave, which it does here between lead V three to V four, that's normal. So there's normal progression. What about ST segments and T waves? The more experience you get with this, the more you're gonna look at groups of leads there is ST depression in each of the inferior leads with an upright, pretty large upright terminal T wave. And I have ST depression that pretty much begins in lead V three V four, V five V six in which lead or leads is the ST depression greatest and perhaps you notice its greatest in V three V four. And perhaps you appreciated these T waves are really pretty tall in these leads. I will draw your attention to the fact that the ST segment is isoelectric, not elevated, not depressed in lead V two. Remember what I said about leads V two V three that normally there is slight ST elevation, this is not normal, this is flat for the ST segment and it should normally be a little bit elevated. If you look at this little schematic, these are chest leads, anterior leads V one V two V three. And and then we get to lateral chest leads. There is no good lead that looks at the posterior wall of the left ventricle. So a lot of people say, well, let's look at posterior leads V seven V eight. But the problem is look at all of this muscle mass and lung space that you gotta get through to get to posterior leads. So it is much easier if you look at the mirror image of these anterior leads. And that gives you a mirror image view of what's going on. The posterior leads. And it just takes a little bit of practice to get used to this. So here is the actual schematic tracing and if I flip it up, that's all I've done is flip it up here. Doesn't this look like what you expect with an infarct? The taller the R wave, normally, the deeper the Q and the deeper the ST segment depression, the more it looks like an acute infarct, that's a mirror test. And with a little bit of practice, you could get used to looking at this. And this was one of the cri that I mentioned when you're looking for, how do you recognize and only there's no ST elevation on this particular tracing, but there is a maximal ST depression in V three V four, these funny looking terminally positive T waves. And if you do a mirror test, doesn't that look like an infarct. Another concept is when you have such diffuse ST depression, you look at this in three of the limb leads, you have them in V three V four V five V six and you have a little ST elevation in VR this is something called diffuse subendocardial ischemia and it can be due to a lot of things. It is not, it is not only left main disease, it could be any type of severe coronary disease or it could even be something that's noncardiac patients with anemia. You got a hemoglobin of, let's say six and hematocrit of 18 that can give you diffuse ischemia or tachycardia cond this or severe coronary disease. So this patient's got a lot of ST segment depression, but the most ST depression V three V four with the positive mirror test and the patient's having chest pain. So this is the patient that you want to consider strongly is having an OM I, I'm gonna show you this followup tracing. This was done 18 minutes later, you could see the nine regular leads and three leads V four RV eight V nine. So they did not, they did not repeat a regular 12 lead E CG. Instead, they got rid of leads. V four V five V six and they replaced them with V four RV eight V nine. And my message to you is if you're gonna do other leads, do a repeat, complete 12 lead and do the other leads cause here we lose what's happening in V four V five V six. Now this is 18 minutes later, the patient's chest pain is now less before we look at these other leads. You tell me what's going on. What do you think compare this? And I will emphasize this is the best way to compare EC GSA. Lot of people they look at one, then they look at the other. You gotta look them side by side because otherwise it's very easy to overlook differences. And if I look side by side, is there any doubt that the ST segment depression is less compared to the earlier leads that the T waves, particularly in the chest leads were greater initially and they're less here and there is now significantly less ST depression here and the patient's chest pain is less. What do you think? What is that? There's a change as well as documentation of change in the patient's symptoms? So, these are dynamic ST dash T wave changes. This is data. I don't even care what the troponin is. I don't care about anything else. This tells me this is an OM I with the good news that 18 minutes later, there probably was some spontaneous reperfusion and this patient needs to have some definitive reperfusion. Ideally go to the Cath lab. So you can do PCI to prevent the vessel from reocclude V four R. It's the best right-sided lead to tell you if you have a right-sided infarction because oftentimes it's hard to tell that and there is no right-sided ST elevation. So no, now V eight and V nine, they do show some slight ST elevation, but I maintain that the amount of ST depression that you saw in V three V four and the amount of abnormality of these tremendously tall hyperacute T waves is much greater than the tiny amount you have here after passing through all the back thick musculature. But the point here this is a serial tracing and I will tell you the overwhelm majority, they never write down what happens to the patient's chest pain at the time. Each E CG is done and they lose all of this stat. Here's the followup of today's case. There was really good care by the emergency medical team. They quickly recognized there was an OM I and OE the oncall cardiologist did do emergency cath. This patient had multivessel disease with an acute blockage occlusion and acute omi the first obtuse marginal branch. This is a branch of the left circumflex artery. So we diagnosed this, basically, we said there was an omi there was a posterior infarction patient has multivessel disease. That's what all of this acute ST depression was. And this was good care by the on care team.