Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hello everybody. This is He Grauer. This is the second session that I'm doing on 12 lead. ECG S. My goal in the 30 minutes that I have available is to make this as user-friendly as possible. Hopefully present an approach that makes ecg interpretation easier for you more accurate, more time efficient. 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. The two EC GS I'm showing you were obtained from a man in his thirties. He presented to the emergency department with chest pain. It began several hours earlier. ECG number two was recorded one hour after ECG number one, ECG number one E CG number two, cardiac catheterization was advised, but the patient refused instead, he left the hospital only to be found dead at home 36 hours later. So how would you interpret these two tracings serial tracings that I'm showing you here? Why did the patient die considering the history? What do these two ECG S show you number one, that the patient did not have an acute event. Number two, that the patient may have had an end stemmy. That's a non ST elevation myocardial infarction or three. That this probably was an o that re occluded. And I'd like you to just take a moment and look at this. We're gonna go over in a second. Each of these tracing sequentially. Let's start out with E CG. Number one, this is the initial E CG in the emergency department. This patient presented with chest pain. So what is my system for 12 lead? This is my 12 lead approach. There are actually six parameters. The first two of which are rate and rhythm then intervals, then axis chamber enlargement and looking for changes of ischemia infarction which I call Q RST segment changes. This does not, does not slow you down. On the contrary, using a system both for rhythms as well as for 12 lead. EC GS, it speeds you up. I do this in real time. And the reason it speeds you up is that people tend to go back and forth and they say, did I look at this? Did I not look at this? If you're using a system, it totally organizes you. It makes you sound like you really know what you're doing along the way, it narrows down your differential diagnosis and you do it in real time. So rate and rhythm. What do you think? And we don't have a long lead rhythm strip here, we can focus. However, on lead two, we see an upright P wave and lead two. And we see a narrow QR s, this P wave is related to the QR S with a fixed and normal Pr interval. This is normal sinus rhythm. The rate is a little bit faster than 75 maybe 80 BPM. So it's a sinus rhythm about 85 per minute intervals. The pr interval is not more than a large box, it's fine. The QR S is not more than half a large box, it's fine and the QTC is clearly not more than half the RR interval. So that's normal. So sinus rhythm, normal intervals, the axis we're upright and leave one or upright and lead. VF it's a normal axis chamber enlargement. I alluded to the number 35 as the best single criteria in my experience for assessing for L VH. Some of the deepest S wave in leads V one or V two tallest are in V five V six. We're nowhere near that. I'm looking for criteria for all of the four chambers. There's no chamber enlargement here. QRST segment changes in this patient with chest pain. I look at all 12 leads for the presence of Q waves, R wave progression and ST segments, T wave changes. I look for patterns of leads. I look for lead areas. So I will look for example, at the three inferior leads 23 and aVF together. And actually this is not AQ wave if you can enlarge this or look closer there's a tiny little R wave. Now, some of you may look and say, but there's AQ wave here. This is an interesting phenomenon leads three and a VF they're inferiorly, I think of them is sitting on the diaphragm. Now, what happens when you take a deep breath in the diaphragm goes down and then it comes up as you expire and sometimes you will see Q waves may come and go particularly in leads three. And a VF I think that's what we have here. Even if this was AQ wave, it's very, very narrow. I can ignore Q waves and AVR and V one cause those are normal. So no significant Q waves here, R wave progression, the R wave tends to get progressively larger until the R wave is taller than the S wave is deep, which normally is somewhere between V two to V four. Here, it's between V three to V four. That's normal. So there's normal R wave progression. Now, what about ST segments and T waves? And I'll let you look at this a bit and you can look either lead by lead or you can look at the inferior leads together. Here's the high lateral leads one and A VL and the chest leads. How many of you just think to yourself think these are fairly unremarkable, but this patient has chest pain. Now, take another look at leads V three and V four and answer the question as to whether you think these ST segments and T waves are normal or unremarkable. If the patient had no symptoms, no chest pain, maybe they had preoperative ecg or something versus if the patient has chest pain. And this emphasizes another point. I really wanna bring home how important the history is in assessing patients with chest pain. Now, how many of you think? Gee this isn't dramatically abnormal, but this ST segment looks a little bit straight, a little bit straight. Take off. This is nonspecific, this is subtle. This is nondiagnostic in a patient with chest pain. To me, my eye says question mark, I could not make a diagnosis from this alone but question mark, let's just store that for a point. And here's the second ECG done one hour after ECG number one. Now remember at some point after this, this patient refused cardiac catheterization, went home and died at home. I want you to look at the second tracing compared to the first tracing. I want to bring up a number of important points. One of the most important of which is how do you compare tracings? This is the best way to compare tracings. I have them side by side. Most of the time when I observe people look at one cardiogram by itself, then they look second cardiogram alone. And if you did that, you may say, hey, this is nothing specific and hey, this is nothing specific. However, if you look at them lead by lead. So this is the best way to compare tracings, get them side by side. Now, the first thing you have to do when you compare is ask, am I comparing apples versus oranges by that? I mean, are these tracings otherwise very similar, if not the same? So I look at the frontal plane axis leads 123 RL NFI, forget about the chest leads and look at each QR S complex isn't the axis just about the same. So there's been no change. Now, a lot of people don't realize that changing the inclination of the bed can sometimes change what the QR S looks like, it can change your axis. And if I had a different axis, I might change the ST segments without, without this being an ischemic change. So we need to make sure we're comparing apples with apples and we are. And if I look at lead one lead, one lead, two, lead, two, lead, three, lead three, I'm going lead by lead, no significant difference between the limb leads. So they look the same. However, what about the chest leads now with the chest leads when we're comparing lead to lead, what we're looking at is our way progression. Because if the technician, whoever did the electrocardiogram takes off the electrode leads after the first cardiogram and say there's a different technician that does the second cardiogram, you will be amazed at how even experienced technicians let alone medical providers who are not strictly EC G techs who do an E CG, how much variation you will have as to where the chest leads are placed. I've been amazed at this. Actually, they're pretty good chest leads are of a lower amplitude. This gives you the standardization what this shows here. This one is half standardization. So that accounts for the fact that the QR S amplitude here is less than what it was before the shape of the QR S complex, however, is virtually identical. So we are comparing apples with apples. What about the ST segments and T waves lead one V one, not that much difference. How about lead V two and lead V three? Look at the relative height of the ST segment and T wave here compared to here. Look at the relative height of the ST segments and T waves here versus here. What's the difference? What do we wanna know about the patient at this time? What do we want to know what we wanna know is if this patient is still having chest pain, right? The patient had chest pain here and remember I said these were nonspecific changes because I've looked at maybe a million ecgs. I think there's some ST segment straightening. But even if you didn't pick up on that pretty un remarkable. But is there a change a relative change? And I submit that there is a change that these ST segments and T waves are a little bit less peak than they were over here. What if it turned out that this patient had no chest pain an hour later? What might that tell you to compare tracings? Correlate each ecg with the presence and severity of chest pain that was not done here. Let's imagine the patient no longer had chest pain. This patient went home, the patient probably felt I feel better. Why should I stay? And the emergency provider may or may not have realized how important that was? Are there dynamic ST segment and T wave changes? I don't know how many of you have heard of that concept. I'm gonna go over it in a second. You could look for a baseline tracing. Now, remember I said to me this is ST segment straightening. If we could have found a baseline tracing, say from a year ago at the time whenever you get a baseline, you gotta know gee was this a baseline when the patient was admitted for myocardial infarction? Was the patient asymptomatic? But if in the baseline, you had a nice, gentle up sloping of the ST segment, you might be able to notice. Gee now they're straightening. That's a difference. And here's the last point until you know, for sure what's going on? Keep repeating GS. How long did the providers wait until they got their second ECG they waited an hour. If you have an actively evolving myocardial infarction, how long might it take until you begin to evolve changes. Now, it might take an hour and it might take a lot less than this, I've seen within 10 minutes or less dramatic changes, particularly if the patient's symptoms are getting better or worse. If you are unsure, continue to get serial tracings until you know the answer realize that sometimes you gotta get them as soon as every 10 to 15 to 20 minutes until you know, for sure what's going on. Let me review dynamic E CG changes. If ECG changes evolve in a way that corresponds to the coming and going of chest pain symptoms, this is important information. It tells us that there may be an active ongoing process and that prompt cath with acute reperfusion is likely to be needed regardless of whether or not the millimeter definition of a stemi has been satisfied. But I think the number of millimeters is irrelevant. So the concept I want to reemphasize is an O by it's an occlusion based M I think about what we care about. If somebody's having an acute myocardial infarction, what you care about and the reason you care about it is if you have an acute occlusion of a major coronary artery time is muscle and you wanna get that vessel reopened as soon as you possibly can. There is data that suggests that the standard use of the stemming protocol results in missing at least 25 to 30% of acute coronary occlusions at least 25 to 30% if you're stuck in the stemi paradigm. And how many of you have worked in settings where the clinician and or the cardiologist says I'm not going to the Cath lab. It's not yet a stemmy. Well, by the time it's a stemmy, it may be several hours later and you may have lost your golden window of opportunity for salvage of a lot of myocardium. So the process of evolving in acute M I is dynamic. There's acute coronary occlusion accompanied, oftentimes not always but most of the time by the onset of chest pain and usually by ST elevation at some point, myocardial damage can be limited if there can be acute reperfusion of the acutely occluded or the culprit artery reperfusion is accomplished medically by acute cardiac cath with either angioplasty that opens the vessels or if you're in a center that doesn't have prompt cath capability, you can use thrombolytic agents. I think angioplasty and acute cath is better in 2023. But thrombolytics may work fine if you don't have that. If the culprit artery is reperfused in a timely manner, the patient's chest pain is usually gonna be at least reduced if not relieved. And usually the ST segment elevation will either decrease and sometimes resolve. This is usually followed at some point in time, later minutes, hours by reperfusion, ST and T wave changes. If the ST segments were up initially, then you may get t wave inversion not commonly appreciated is that reperfusion of the culprit artery will often be spontaneous even before medical personnel arrive on the scene. So the patient complains of chest pain, calls ems to get to the scene. Patient says, hey, my chest pain is better. Well, maybe it wasn't an infarct or maybe it was acute coronary occlusion and now it's spontaneously reopened. So this is where the history gives us clues that maybe there was spontaneous reperfusion. If the chest pain is suddenly reduced or relieved, and if you can get on a cardiogram, that corresponds to that and show that the ST segment elevation is less when the chest pain is less, then you've pretty much shown until you prove otherwise that you have an O regardless of whether you ever had enough ST elevation to qualify by the semi definition. The problem is that what's spontaneously open may just as easily spontaneously reocclude. So this is why if you can diagnose that there was acute coronary occlusion that there was an O that then spontaneously opened that patient, even though they feel better, even though the ECG may now be pseudo normalized. They need a prompt, Cath with PC or some other intervention to prevent spontaneous re occlusion. This is our survey I've reproduced. We'll assume that the patient's chest discomfort had been reduced at the time of this. What do you now think happened? Use of the term nstemi or non ST elevation M I in many ways. It's a useless term. In my experience. It's a grab bag diagnosis after the fact. And many of those patients actually had an o here, if troponin was up, the provider may say, gee that was an end stemmy because we don't see the ST elevation when in fact, if the troponin is up and here you had chest pain and here the chest pain was relieved. That was an only. And if you're there, that patient needs to go to cath and ideally repeating, the cardiogram should have been done a lot sooner. Last minute, hyperacute T waves. This one is not obvious in retrospect, this was hyperacute. But even if you didn't know that there were dynamic ECG changes weren't there. So the lessons to be learned from today's case, what is meant by dynamic ECG changes? We have correlation with symptoms that changed correlation to the E CG. Even though criteria for STEMI were never obtained, this shows dynamic changes that by itself should be, should be enough documentation and indication for cardiac catheterization. So we went over how to compare serial tracings, how to diagnose and recognize dynamic ST segment changes. The most likely reason this patient died was what that they had an that spontaneously reopened patient went home. It spontaneously re occluded potentially could have been prevented. Last point. Can we determine a culprit artery? Again, this is subtle. This is a nonspecific ecg but this shows changes that straightening and taller T wave, it shows it in the anterior leads, that's the L AD distribution. So I would say this is a probable L ad the only acute L ad occlusion. And again, not diagnostic. Absolutely. But given that history, this patient needs to go to the Cath lab as soon as possible until you can prove otherwise. I suspect they would have found acute occlusion of the L AD.