Chapters Transcript Video EKG Review Click here to view presentation deck Back to Symposium My name is uh Dan Thibodeau. I'm part of uh center cardiology up in Williamsburg, but I'm also a professor at uh formerly Eastern Virginia Medical School. It's got a long name now. Um Thank you for all you do for your patience and your community. And uh what I'm going to try to do this will be a little bit of a rapid fire just to remind you of some things that you need to think about with uh EKG S. This is not an all encompassing course on EKG S in 20 minutes, of course. So um happy to share my slides if you just email through my Centa email, happy to send you a PDF of all these slides because some of them uh we're talking about small squiggly lines. So you may not be able to um see them as well, but we'll try to talk about patterns and waveforms and describe some of these typical findings and then we'll talk about improving uh pattern recognition. So, just with fundamentals. Um one of the things that I was taught early on uh actually by George Sarris who's also part of Centa cardio, we've known each other for more than 20 years. He uses this phrase that he learned in fellowship, regular or wide, fast or slow kill my patient. Yes or no. It's a very simple thing to think about when it comes to looking at an EKG, when we're looking at our QR S complexes and any possible changes that might involve ischemia or any other abnormalities. So you want to think about that in a very simple way. Uh But keep a process when you read EKG S and keep that methodical approach because I think that's how you uh reduce your things of missing uh uh tracings uh and especially pulling up prior tracing. So you can compare one to the other. It's always very helpful. Did something change from the last time you've had this and that's also in the acute setting as well. Sometimes patients will evolve right in front of you. And so having a repeat tracing can be uh very helpful, especially uh if they're having active symptoms and then when it comes to arrhythmias or you have a concern for arrhythmia, just have one of your technicians just perform a longer rhythm strip while you're there. Sometimes looking at trends is a lot helpful than just one page of an EKG. So just reminders of your intervals because your intervals are going to be important to recall of where everything fits within the EKG and understand that those intervals have certain times uh that are associated with each uh interval. So your pr your QR s uh your uh and and ST segments. It's especially true when we start thinking about medications that can alter these types of, of segments. Uh And we'll talk a little bit about a long Qt syndrome as well. That can happen. One of the things that I think uh we have to remind ourselves is the action potential of what's happening to the sodium potassium channels as well as calcium and how that impacts uh electrolyte changes with regard to what the EKG is actually showing. So when we superimpose uh a regular EKG B, you want to think about where these channels are, are opening and closing. And then when we think about electrolyte abnormalities and rhythm disturbances or changes, we have a better understanding of why that occurs. So we want to think about that with respect to electrolytes. Keep in mind that there's a process to a 12 lead EKG where we initially started with Eindhoven's triangle with the bipolar leads. Uh And then we did our augmented leads which are unipolar and then we have our chess leads of our precordial leads and always a rhythm strip on a 12 lead EKG. Now these can be variable uh depending on the machine. Sometimes there might be three rhythm strips on the bottom as an example. But keep in mind what you're looking at and what that means. It also is relative to when we talk about the zones of perfusion and we'll get into that a little bit more. Uh later this uh talk, when we talk about access, some people don't even think about it. All I want you to think about is an axis, is the summation of where the electrical forces are heading. And if we have a normal axis and a normal heart, what we're, what we're going to have is a zone as an, as a region of where those impulses are heading. And so we know that the chest, uh the heart doesn't sit perfectly like this even though we all do these things. And um the, the heart sits where the right atrium is more anterior, the left ventricle is more shifted to the side. And so instead of it being exactly like this, it shifted backwards like so, so when we get to talking about polarity, that's why leads one. V one and V two are negative because they're on the negative pole, they're going this way, we get into our isoelectric line right around V three. And that's why we normally see isoelectric activity at V three. And then once we get past V 345 and six, we have a positive relationship to the EKG on the precordial leads. So it's important when we think about access, we also think about our way progression. So we should be negative for V one and V two isoelectric V three and then we turn positive and that amplitude we should see in a normal EKG. So when we think about why access can matter, we think about abnormalities to the, the substrate and how that can change based on disease. And so the simple thing I want you to think about to read access as part of your reading is think of leads one and two and so leads one and two are positive. You have two thumbs up, we're OK, we're in a normal axis. And as you can see, we have different access determinations depending on certain diseases that occur. And this is how we want to look at um our, our tracing to determine has the access changed from the last time you've had a tracing if that's available. And what does that mean for the patient? What has happened? And so we put it in a very simple way of looking at it in degrees and this is where we used to read uh access in degrees, the machine does it for you. But it's important to remind yourself of where that fits. So at a, as a, at a very simple approach, I've added this uh part of the screen and that's why I'm happy to share these because we're going a little fast. But the simple approach is looking at leads one and a VF is another approach that you can do and it can tell you what your access determination depending on the positive or negativity to those uh leads here's an example of a left access deviation where you see that um one is positive, but you have 23 A VF as negative. So you've had a change in access, which likely implied that the patient probably had uh an, an infarct at some point in time. So when you see these types of things and they're different from what they were in the past, you can uh understand that something has changed And that's an important part uh of your uh asking the patient in history. Now, when we talk about wave forms, um P waves can happen uh in various uh uh formations. Uh sometimes they can be notched, that can be a normal variant. But one thing in primary care that uh certainly uh is hard to uh address early on are things like heart failure. So a bias P wave can sometimes be the early identification of possible heart failure in that patient that you've treated with hypertension for years. And so those little subtle changes can be um can be uh indication that something might be happening. But realize that the P wave can look very different uh in morphology. Some of these can be normal variants. But it's a clue to say, is there an electrolyte problem? Do we have a remodeling of the atria that could indicate there's something else going on? Same thing with the QR S complex. So we want to have that duration less than 0.1 2nd. and um depending on the, on the ventricle size, uh your QR S complex can be a larger amplitude. This is especially to a young healthy individuals. But when we start seeing changes from a prior tracing where the amplitude is getting high larger, it may start implying ventricular hyper hypertrophy, which we need to be aware of. And so we need to be mindful of this when we're looking, but also realize that QR S complexes can change over time and that they can mean a uh a varying uh of different types of abnormalities that can occur from um like Dr Patel mentioned with uh early reentrant uh problems with WPW, you could have um uh widening of the QR S from uh idioventricular delays. We'll get into that a little bit later or you could have bundle branch blocks that occur over time. So your, your QR S complexes can be very different. Your ST segment should have a normal process where the ST starts at the baseline, where your pr comes across. You should have your ST start right at that point as well. And so you kind of remind yourself where your baseline is and then you can evaluate your sts depending on what you see, but you can have various wave forms depending on factors of early repolarization in young healthy hearts. You can have um hypertrophy of uh or hyperkalemia uh related to uh electrolyte abnormalities or you can have ischemic changes. And so it's uh it's important to recognize these changes when it comes to the ST segment. You don't really see U waves that much except in um slower heart rates. These are usually considered to be after uh depolarizations, they don't really have a big significance to them. But every now and then someone might uh identify that and think it's a P wave when actually it just might be a U wave and a slow heart rate. And so something to think about, I mentioned repolarization. Uh Usually we see this in, in, they are normally global. So you will, you should be able to see these across the entire EKG. Usually young, healthy individuals have these uh and um uh they uh are able to just snap back the, the myocardium uh because of the healthy heart. Uh and it's something that we have to think about. Usually this concavity uh normally means that the substrate of the heart is usually fine. There's usually very little uh disease associated with this, but sometimes we'll see individuals referred to us by this early repolarization mo uh model. Uh and it's perfectly fine different from ST elevations, which normally we will see in situations where patients are actively having symptoms like in sties. So it's a difference in how it looks. So this is a good example of early repolarization. And if you look through the entire precordium, um OK, the pointer doesn't work. But uh if you look at this throughout the entire Precordium. You see that the, the uh the ST, the J point starts very early uh and it works itself all the way through the Precordium. It's a little bit more reassuring when you see this different from other types of, of situations where the ST the, the S portion is already started and then you get big T waves. This is where you already get that ST starting right at the before the J point uh and showing early repolarization uh models. Let's talk a little bit about bundle branch blocks. We're just talking about abnormal block of conduction which can delay the QR S pattern, uh both on the left and right side. And so we have to recognize that what we will see with these bundle branches is we'll see a delay. And in the delay on the right side, we normally get the classic bunny ears uh uh pattern which you typically will see at least in V one in some cases V two and V three as well. But you should see it in V one. You'll see a slight slurring of the uh S wave in V six as well as lead one. Alternatively with left bundles, you'll have the, the opposite where you'll see this pattern widening. And normally I want you to think about a rock being thrown up uh and falling with that uh left bundle branch block, it goes all in the same direction and it usually goes in the same direction um uh uh of, of the P wave. Um And you'll see that reciprocal change in V one with the slurring of the S wave uh in a left bundle. Here's where uh it might be a little bit difficult because of the distance. But uh I tried to make pointers of where those abnormalities are relative to a right and left bundle branch. You can see where you have the slurring of the S waves in V six for a right V one for a left. And then you see your CRS with a little bit of notching on the uh left bundle branch of V four through six. And then you see the classic uh bunny ears uh uh through uh one V one through almost the four, there's a small little notch there. So these are typical patterns that you see. Um It doesn't necessarily mean that the patient has a pathologic uh disease that needs to be addressed right away. It's something to watch. Uh But new left bundle branches in, in the presence of possible ischemic uh complaints is something that we have to have a little bit more concern on and you might need to do a little bit more of a deeper work up in those individuals over the course of time. We all hope that individuals will stay in the green zone uh uh all the way to the left. But at time as uh we, we age and uh disease progresses, we get different types of blocks. We initially start with incomplete blocks. Uh But then as the disease uh has the potential to worsen, we get into a complete and most of the time irreversible condition where you get a, a third degree or complete heart block. When it comes to a first degree A V block, we're starting to talk about uh apr interval That's usually greater than 0.2. Uh, we have to think about medications like beta blockers, calcium channel blockers in some cases, digoxin as possible, culprits for this. Uh, sometimes in, uh, it, it's, it doesn't happen often but in ischemic conditions, um, the pr interval could be widened. But if the patient is asymptomatic, I would look at the medications first determine if there's anything that the patient might need to come off of to see if that improves it. Otherwise, it's something that we just watch gets a little bit more problematic as we go on with Mobis, uh, type one. And we'll talk about Mobis one and MOS two mos one is where we start getting a progressively widening pr interval with then eventually a dropped QR S. So we have a progressively widening Pr with a drop QR S. And so as you can see here, we have, um, uh, slight, slightly wide, goes to wider and then at some point, it doesn't always have to happen right away. You drop a QR S and then you have the pattern that will repeat it again. And so this is why longer rhythm strips can sometimes be helpful in these situations. Same situation. Look at their medications, see if there's anything that potentially could be, uh, uh, the culprit for this, have them come off of it. If they are symptomatic or they've had issues with uh syncope or near syncope, might be a reasonable thing to investigate with Halter or uh um uh loop recorder uh for longer runs to figure out if we've had uh any abnormalities there. With Mobis two, we don't have the progressively widening PR S. Now we just have random drops of Q RSS and that can be in a, in a uh a repeating pattern. Other times it can be a random uh occurrence. And so what the difference between the Mobis one and the Mobis two is that now you're just getting a random drop of the QR S. So we're progressing along with the disease of our electrical pattern and then we eventually can have individuals who come in and sometimes they come in. The, this is the first time you see them where they have total dissociation between the atrial and ventricular uh um uh patterns. Uh And so with this, you will see that the P to P intervals in this particular case, are totally independent of the QR S complexes. A lot of times patients will be symptomatic with this the big issue is are they hemodynamically stable or not, that will sort of raise your, your concern of, of how they get approached. Uh If uh but if you see this in your office, this should warrant um getting a als transfer over to the hospital for further evaluation most of the time. Uh these are irreversible and so these individuals will require a pacemaker to get it back on condition. Junctional rhythms and idioventricular delays can occur. Uh And it's junctional would be without the presence of a P wave. And because you don't have the electrical activity, it goes right to the ventricular rate. And this is why junctional usually occurs with bradycardia. And that's why you get a ventricular rate that is lower with the absence of a uh the P wave junctional bradycardia. The QR S complex is usually always narrow different from an idioventricular delay where you don't have a uh P wave at all. But your QR S complex uh becomes a little wider and that's the difference between the two. So, keep that in mind when evaluating your tracings, we're going to get into a little bit of disease specific and how am I doing on time? We're good. OK. All right. So, one thing that we need to think about when I talked about the action potential with electrolytes is uh if, when we have conditions of hyperkalemia and other electrolyte abnormalities, this is a patient who actually has hyperkalemia in the setting of acute renal failure. And so you can see how we have uh uh a little bit of a widening of our QR S pattern. But we also have hyper QT waves. And so when we see these types of, of, of things, and especially once again, I I keep repeating, this is look at the prior tracing that gives you a good indication, has something changed. And in this case, clearly, the patient has slowed their heart rate. QR S has widened their uh hyper acute uh uh T waves uh which is an indicative of hyperkalemia. One thing that we saw a decent amount of uh uh uh throughout our uh pandemic and COVID were uh postinfectious pericarditis. Um We have uh global ST segment elevations. Sometimes individuals um may um think that these are stemming. But what we have to look at is that with pericarditis, all leads have global ST segment elevations. Patients will come in with uh chest pain complaints. And I think that's sometimes why they get uh concerned for a possible ischemic uh problem. But usually these are individuals who are having symptoms for a longer period of time in general. Uh But we need to think about the situation of why this would occur. Certainly our, our viral infections and um are are the most common. Uh but young uh healthy individuals can ev every now and then get these through uh um you know, minor uh flu, uh uh flu, uh illness or uh in some cases COVID. One of the things that can happen in the classic patient is in COPD is multifocal atrial tachycardia. Once again, having an appropriate approach to reading an EKG. Looking at your, your morphologies of your P QR sts is very important and look at patterns of, of, of the rhythm as well. In this case, those three arrows point to the P waves. And if you look at those P waves, if you can see them, all three are different morphologies where you have an inverted uh inverted P wave, you have a hyper acute P wave and then you have a bias P wave all in the same um patient. Uh And the rate happens to be a little bit faster, which qualifies for MA T one little pearl. I want, I might want to add to reading EKG S is that one lead does not necessarily mean that you have a rhythm disturbance by reading one lead. And so remind yourself that all of these leads are being traced at the same point. So it's the same beat. And so what you uh is helpful sometimes and I teach our students this is don't focus just on 11 lead, go up and down and make sure that, that tho those P waves are consistent, that the Q RSS are consistent because it's the same beat uh from bottom to top uh all throughout the EKG. But when you see different P wave morphologies in this instance. Uh ma T is um uh the likely diagnosis. Uh And the good part about this is that there's nothing electrocardiographic that you need to do as management. You, you are treating the underlying disease of what is causing it. Uh Doctor Patel, I won't mention this much, but Doctor Patel mentioned WPW with uh classic uh delta wave formation in the beginning of the QR S complex. These are generally younger individuals when they early get diagnosed, late teens, early twenties, most of the time, uh uh more females than males and African Americans more than whites. So kind of keep that in mind, especially in situ situations like Doctor Patel's uh mentioned with palpitations um and uh possible uh episodes of uh syncope with no clear understanding. One of the things that can get missed from time to time is when you have Long Qt syndrome, when your, your QT is greater than 440 usually in men, 450 to 460 women uh is um is, is thinking about individuals that make uh be sluggish consume themselves to be a little weaker at times. Uh And we need to consider that long QT could be a possibility of why this is happening. The list is long and distinguished on what could uh cause these. But pharmacologic is certainly at the top of the list, excuse me. But there are also some uh genetic and congenital abnormalities that can occur. And so, uh, long QT, if it's not corrected by simple electrolyte, uh, abnormalities or medications, uh, then you need to think about, does the person have the possibility of a genetic disorder that could be causing it? Uh, like I mentioned, the list is long and distinguished on medications that have the potential to cause a long QT. Uh, and it's something to think about some of the, uh, antipsychotics. Uh, we don't use as much these days. And then our tricyclics, we have not used uh as frequently, but we every now and then have patients who have been on them for, for years. So something to think about when we talk about long QT. And then lastly, I wanted to mention about ischemic changes. We all worry about missing something when a patient comes in or they're having symptoms. Uh And so sometimes it can be a little bit of a challenge of where to gauge what, what's wrong with the patient. So there's sometimes the little subtle things that we should look for, but also will demonstrate uh some of the abnormalities that we can commonly see when patients are having symptoms or they've had problems. Uh This slide is just to kind of keep in mind uh, zones of perfusion and where we would have uh possible changes that come together in more than two, usually more than two leads. So we think about contiguous areas and zones of perfusion. So uh 23 A VF is our classic um inferior leads. And then we have our anterior leads from V two through four. And then we have our lateral and we call these in, in, in some cases low lateral V five and V six. And then you have your high lateral leads, uh which you uh every now and then we'll see it in what we call reciprocal changes. And I'll have a few slides related to that. But what we'll have is different changes of the ST segments based on timing of when uh ischemia may have occurred or initial injury, uh from a perfusion deficit. And so as you can see things will change immediately from just seconds. Uh and then as it progresses, you start having, uh, start to uh witnessing um larger changes to your ST segments based on uh how the degree of uh perfusion has been impacted, uh and where that perfusion deficit is occurring. And then of course, uh from uh days to weeks, patients are starting to queue out uh as part of that. And you start the scarring process uh in the myocardium. Keep in mind that under uh different uh areas of stress, you can have ST segment changes that can occur uh in, in various patterns. Uh And so something to think about when individuals are, uh having uh tests like this, uh stress tests are just a walking test where they might be hooked up to, uh a holter and they're having symptoms. We talked about uh convex and concave shaped uh more concerning for the concave uh uh pattern uh where you worry about ischemia, where convex doesn't necessarily mean you're having ischemic changes. And in most cases it doesn't. So one of the ways that you can think about it is the, the happy and sad face of what uh has the potential to be a little bit more worrisome than others. So the con convexity is a little more worrisome than the concavity, uh which tends to not have as much ischemic components to it. And here's a good example of those changes under stress. J point elevations can occur as well. Uh And we have to think about the possibility it can sometimes uh occur in normal individuals, but we certainly have the po potential for early ischemic changes with J point elevations and something something we have to uh be mindful of. But STST segment changes can be um subtle from the start. And so this is once again looking at prior tracings and what that EKG looked like uh can be uh very helpful, but the ST segments can be as simple as just flattening out of the ST where you have a change uh along with patients might be uh might be having symptoms. And something that we have to think about when we compare the uh uh sts could be flip Ts uh as another pattern uh recognition. And certainly when we have individuals that are complaining of symptoms, it's a little more uh put, put a little bit of, of, of a little bit more investigating into that when you're talking with your patients, when we start getting into changes of stress, especially when patients are actively having symptoms, we think about that change of our ST different from the baseline of where that pr interval starts. Uh And so as patients are having uh more symptoms, you can have changes where uh the, the ST segment will depress like. So in this situation, we have large ST segment uh changes to the inferior leads. As you can see with 23 and A VF we also have um this occurring through uh V one through V four. There's always the possibility of a posterior component to this from V one and V two. If you flipped it over, you'd have ST segment uh elevations as a possibility. But you can see also that in leads one and A aVL, you start having some reciprocal changes that I mentioned before. Sometimes uh patients will have global ischemic changes uh where you'll have large uh ST segment uh T wave inversions. And you can tell that this individual uh in this particular case, had a history of global ischemia, this was actually their baseline. And so this is where um having prior tracings and understanding where, where the patient uh uh lives with their uh prior tracing can be very helpful. So you understand where you're going uh with uh their management. But uh like I mentioned, reciprocal changes do occur. Um and they're a result of just the polar opposite uh zone uh that we're talking about, that's just reacting to the acute problem, which is in the inferior leads. And so then the other uh ischemic changes that become a little bit more concerning are when you start having large, larger ST segment elevations and more than uh in, in two contiguous leads or more. Uh usually the, the, the, the cut off is uh at least two millimeters. Uh But put that in the context of how the patient is feeling and, and what kind of symptoms they're having. This is where repeating EKG S uh can be very helpful. I've seen individuals who have had EKG S uh like this where they're having some symptoms, five minutes later, I'll repeat it and it's, it can be a sty. So that's why repeating EKG S can be extremely helpful. Uh because these are the things that are unfortunately that occur where you have large ST segment elevation stemi. Uh there's an anterior stemi uh with large tomb stoning effect of your ST segment. So things to think about um the other thing that I would mention in, in the situation of ischemic changes is when you have individuals that are still having active pain, they're having ST segment changes and then they start throwing PV CS when you have situations like that, uh, usually indicates that you might have an anatomical problem that's causing those, uh PV CS to occur. Uh It should heighten your awareness that, uh you have a greater concern that something acute is happening and that uh, the patient needs to be evaluated sooner than later. So your clinical, uh, considerations are the, the patient's symptoms, their history, uh, your risk stratification should always be part of that. Uh Have they had any prior history of cardiovascular disease surgeries, procedures? Any prior EKG S we talked about certainly your medications, drug to drug interactions can be very uh considerable, especially in things like um uh electrolytes, um QT uh and other uh abnormalities that can occur. So keep in mind of those things and then when the patient has an increased CV, risk, uh worsening CV, symptoms or complaints, um, you've, you've done a work up, you started with echoes or stresses and you start having abnormalities to these, um or you have multimedia management, especially with cardiovascular disease. Um You certainly want to think about when to refer that patient to uh cardiology so they can co manage uh with you on these uh patients that can sometimes be a little bit more complicated. So I'm happy to share those slides. Uh I appreciate your time. Uh uh just uh email me through this tera system and uh I'm happy to give you a little PDF of that. And thanks Published November 5, 2024 Created by Related Presenters Daniel T. Thibodeau, PA-C Cardiology, Physician Assistant, Physician Assistant View full profile
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