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Hello everybody. This is Ken Grauer. This is my third and my last session on ECG interpretation. My dual goals in this session are first of all to go over a systematic approach to interpreting any 12 lead ECG with the second important goal of being how to assess 12 lead EC GS for the purpose of looking for ischemia, acute infarction and especially acute coronary occlusion. All you do is substitute the blog number to have a user-friendly link to get you right there. But let's get started with this case. This ECG was obtained from a man in his sixties who described the sudden onset of chest tightness that began 20 minutes earlier. But who now at the time that this ECG was recorded was no longer having symptoms. So he's no longer having chest pain in view of this history. How would you interpret this E CG? And the key question being, should the catheterization lab be activated? Does this patient need a prompt? Cath, given this particular history man in his sixties, chest tightness begins earlier, but the chest pain is now gone at the time. This E CG is done. Should the Cath lab be activated on the basis of seeing this E CG. And the choices are no because this is not a stemmy, ST elevation, myocardial infarction. It's not a stemmy because there's not enough ST elevation or no because this chest pain is gone. The patients no longer having symptoms or yes, the Cath lab should be activated if the initial troponin value, which is not yet back if the initial troponin value comes back positive or yes, the Cath lab should be activated because this is an acute only. But what I wanna do now is to shift gears and interpret this ecg systematically. I talked about the system that I favor. It's an ECG blog 205. I emphasize that there are six key factors to look at which are the rate and the rhythm intervals, axis chamber enlargement and looking for Q RST segment changes the rate and rhythm. You wanna watch your P's and Q's in the three Rs. Are there P waves or evidence of atrial activity is the QR S wide or narrow in the three Rs or whether the rhythm is regular, what the rate is. And if P waves are present, whether or not they are related to neighboring QR S complexes, there are three intervals, the pr interval, the QR S duration and the QTC, the frontal plane axis chamber enlargement in any of the four chambers. And looking at all 12 leads for the presence of Q waves, R wave progression ST segment and T wave changes. And we're gonna follow this systematic approach, but today's tracing in just a moment. But the point I wanna emphasize, I don't care if you use my system or somebody else's system. But the key point is regardless of what system you favor for interpreting 12 lead Ec GSI want you if the QR S is wide to find out why the point of this is, you've got to look at intervals early in the process. And the reason you wanna look at intervals before you get to access chamber enlargement and Q RST changes is that if the QR S is wide, that your criteria for assessing the axis chamber enlargement and especially looking for changes of ischemia infarction will be different if you've got some type of conduction defect. So you wanna know this early in the process rate and rhythm. Now, we do not have a long lead rhythm strip, but I can focus on lead two. Here, I can see that there are upright P waves. The rate is kind of slow in the mid FF. So sinus rhythm and what about the intervals? So the pr interval is normal. It is not more than a large box, not more than 0.20 seconds. The QR S is narrow, it is not more than half a large box, not more than 0.10 seconds. And the Q TC looks to be normal. I will look at any lead with the QT interval appears to be longest and it's clearly not more than half the RR interval. So the intervals are normal, the axis we are upright in lead. One were a little bit negative in lead. A VF we are actually a little bit more negative in lead two. It's actually a left anterior hemiblock chamber enlargement. There's none, this shows you normal standardization and there's no chamber enlargement. No LVH here. And now we're gonna look for Q RST segment changes. And I like to go through all 12 leads, looking for Q waves, R wave progression, ST segments and T wave changes. Now, the more experienced one becomes, you'll find yourself looking at patterns of leads. For example, I tend to look at the inferior leads 23 and A VF together Q waves. So let's look for Q waves. Do you see any Q waves at all here in this 12 lead ecg? Now, A VR we don't care so much about Q waves because it's normal to see them. How many of you saw that there is AQ wave in lead A VL. And if you look at it, the QR s is really very small here. Compared to this QR S, it's actually a fairly wide Q wave in lead A VL. So this might be significant, easy to overlook unless you were systematically looking for Q waves before you got to the ST segment and T wave changes. Now, what about R wave progression. Normally, the R wave tends to get taller as I go across the chest leads and usually somewhere between leads V two to V four, the R wave becomes taller than the S wave is deep. That's called normal R wave progression. We probably have this but beyond the course, since this patient did have chest pain before these R waves are really pretty small for these first three leads. If we get to thinking about the possibility of an anterior infarction, if I've got really tall R waves in V two, especially V three, then it's less likely that I've got an anterior infarction here. We do have R waves. These are not QS complexes, but they're relatively small until we get to lead V four. So that may or may not be of some significance. But what about the T waves? And this is really the key point? What do you think? Do you think they're normal? Do you think they could be repolarization changes? There's a tendency to call these upright T waves repolarization changes. So the T waves, they're really kind of peaked. They're really kind of tall. What about the ST segments? Is there any ST elevation now, to judge ST elevation? I wanna look for the preceding pr segment. There is a little ST elevation. Now, normally V two and V three are a little bit different than the other chest leads because normally there's some slight ST elevation, there is some elevation here. Not a lot, maybe a little elevation here again. Not a lot. T waves inverted in lead aVL. So that's my descriptive analysis. Now, let's do my clinical impression this patient had symptoms, chest tightness that began 20 minutes earlier but is no longer having them at the time of this ecg. In that context, this patient did have chest pain. That's why they called the MS. They were having chest pain before and it's gone. Now, what do you think of these T waves? How many think these T waves look taller than they should look taller than you would expect them to look given the amplitude of the QR S in these particular leads and particularly given the amplitude of the R waves in these leads because this T wave is even taller than this R wave. And it's as tall as this R wave here. These are hyperacute T waves, these T waves, they are clearly taller than expected. They have a much wider base than expected and this occurs in almost all of the chest leads as well as in the inferior leads in a patient that has new symptoms enough to call ems. These have to be interpreted as hyperacute T waves. Again, you could think about this history. Chest tightness began 20 minutes earlier. It's now gone at the time of this ECG. And it turns out that there was a second ECG recorded ECG number two was actually done first at the time the EMS unit arrived at the patient's home, at which point the patient was having severe chest pain about 20 minutes later. That is on the way to the hospital, the patient's chest pain resolved. And that was ECG number one, I did this intentionally for instructive purposes. Actually, it's what occurs often in clinical practice because it's common if you're working in an emergency department that you don't initially see the ECG that was done by EMS at the scene until a little bit later. Sometimes the first ECG you see is the one that's done in the emergency department. What do you see here? And I think from across the room, everyone would say, hey, this is an obvious sty, tremendous ST segment elevation across all of the chest leads here. We've got ST segment depression with those PT waves. So this is an obvious stemmy. This was done when the patient was having severe chest pain. And then 20 minutes later, the chest pain was essentially gone. That ST segment elevation was almost completely gone. The points I wanna make with this, the clinical reality, all too many clinicians across the world still remain stuck on the semi power dim. This includes all too many cardiologists, in my opinion. Does ECG number one qualify as a stemi? It's kind of borderline could be a stemming. I mean, we have the ST elevation here but those leads normally have it maybe, maybe not. Does it matter if that an initial ecg that I showed you is this stemmy or not? No, it doesn't why not? Because, because this initial ecg is clearly an O it's clearly an acute coronary occlusion in this patient with new chest pain. What do we care about? We care about whether or not the patient has an elevation of troponin from an acute infarct that's due to acute coronary occlusion because those are the patients who can benefit the most from active intervention. Now, if you don't have 2473, 65 I have cath lab availability, then a thrombolytic will work most of the time. I'm not quite as good as cathing the patient and doing percutaneous intervention. PC. But thrombolytic therapy will work fine if administered in a timely manner. The point is use of the Stemi protocol at least 25 to 30% of all acute coronary occlusions are missed if you're stuck on the stemi millimeter based criteria not commonly appreciated. This is key is that reperfusion of the culprit artery will often be spontaneous even before ems or other medical personnel arrive. The history can give us an idea that you've had the spontaneous reperfusion. So the body can reopen spontaneously and you often get a clue to this because all of a sudden the chest pain is lessened or it goes away and you do a repeat E CG and the ST segments are much less. The problem is that what spontaneously opened may just as easily spontaneously reocclude because the process that caused the acute occlusion is not yet taken care of. And this is why with a patient like today who has resolution of their symptoms, presumably acute coronary occlusion that then spontaneously opened. That's the reason why even though the patient's chest pains resolved, they still need a prompt intervention. Ideally, prompt Cath with PC. And your goal here is to prevent reocclusion because otherwise, what sometimes happens is you have spontaneous reperfusion and then spontaneous reocclusion and back and forth until the final stage is reached. So what do you think happened in today's case? And I already alluded to this, the chest pain is gone, ST segment elevation. It's statically reduced here. You could still kind of see those T waves. What do you think the ECG might look 5 to 10 to 15 minutes later? If we repeated it another time, those peak T waves might then be much closer to the baseline on their way to eventually inverting. Now, points from this are several note that it's only 20 minutes between this and this in an actively evolving process. It might not necessarily take much time. What if you only had that ecg that I showed you to look at? What if there was no ems ecg the chest pain is gone. But these are still obviously hyperacute T waves markedly abnormal in multiple leads. It doesn't matter what the initial troponin is, there's no sense waiting. The point is that initial troponins can actually be normal, even high sensitivity ones. If you have a very brief period of total occlusion, before you get the spontaneous reperfusion, the troponins may not yet have elevated. You realize that even if the initial troponin was negative, that doesn't rule out anything. And until you prove otherwise by an acute cath, this is an acute oy, this patient needs an intervention case conclusion, timely, cardiac catheterization was done in this patient but it was the proximal L ad that was occluded. There was successful reperfusion and PC was performed lessons to be learned from today's case include that you have a semi paradigm that is still being followed, but it's outdated for now. Use of the only paradigm because if you're waiting for millimeter ST elevation by the semi paradigm, you're gonna miss 25 to 30% of infarcts. If the patient presents with new chest pain, the T waves. And that first ECG that I showed you cannot be interpreted as normal. They are hyperacute. It's an O remember how quickly this evolved, this only took 20 minutes. And the key is to correlate the patient symptoms at the time of the ECG because it's a whole lot easier to make sense and put together these clinical events into a story that makes sense of somebody who had an acute coronary occlusion that's spontaneously reperfused and that's in need of prompt intervention.