false
Catalog
Session III: Invasive Diagnosis and Treatment-6155
Wide Complex Tachycardias
Wide Complex Tachycardias
Back to course
[Please upgrade your browser to play this video content]
Video Transcription
This is Sam Masurvadam, one of the electrophysiologists, Mayo Clinic, Rochester. So we're going to cover a variety of topics all related to background knowledge on wide complex tachycardias. We'll spend about 20 minutes going over the issues of ECG interpretation, and then another 10 to 20 minutes looking at what the invasive cardiologist should take from the ECG world to their invasive practice. So sometimes we tell our trainees that any book ever written on electrocardiography or ever will be written is all hidden in this statement. Electrical force or vector, when it moves towards the positive pole of the ECG lead, you get an R wave, an upright recording. If it moves away from the positive pole, you get an S wave, a negative wave. So once we understand this principle, we just need to remind ourselves where the positive electrodes are. And we know lead one, AVL, left side, 2,3-AVF, inferior feet leads, and AVR, AVL, kind of derived leads that we could think of somewhere near the shoulder or ear of the right and left sides. Reminder about the chest leads. They're unipolar leads. All are the positive electrodes. They're all on the anterior chest. And note that they are low in the chest. Even the highest of these leads, V1, V2, are relatively low. And in a sense, they just straddle the apical region of the heart. So positive, anterior, mostly leftward, and relatively low. Based on this principle, we can kind of figure out some variations of positive. Little positive vector doesn't start too far away. Focus not too far away from that positive electrode. Very positive, starting very far away and moving towards the positive electrode. If it skims over, then it may become positive and then moves away, could be negative. It's possible to get minimal or no deflection on a bipolar lead if the vector is perpendicular. So say an apical PVC going up towards the head in lead one could be hard to see any kind of deflection. So just a little test of the skill. If you have to look at this ECG, paste electrocardiogram, all of you should be able to match this ECG with a fluoroscopic view, where you can see the pacing lead. So you note, for example, V1, a right side lead is positive. Lead one is negative. One, a left side lead is negative, moving away from the left. So there's left sided pacing, left ventricular pacing. 2, 3 AVF are negative, so more inferior. So inferior or posterior, but lateral pacing lead in an LAO view. This is where you should be picturing that lead or site of activation. So basic skill that we'll use over and over and over again in our practice as electrophysiologists, device professionals. Now this information is necessary for answering question number one, that is, how can we tell with a wide complex tachycardia whether we're dealing with a VT or an SVT with aberrancy? We've heard, read, and studied methods right from medical school about this problem. And using principles of electrocardiography and some clinical information, you can have an easy to recollect usable approach that I'll present to you, rather than memorizing some fairly complex algorithms. So typical scenario may be consulting in the emergency room and you get an ECG like this. How do we look at this? A very seasoned person will probably take a few seconds to come to the diagnosis, but having an approach that will help in any case to give you high odds of figuring out, should you approach this as a ventricular tachycardia or an SVT with aberrancy? And let's look at some of these. First is we have to understand why a QRS can be wide in a wide QRS tachycardia. So why is it narrow with a normal conducted beat? It's because of our unique conduction system. Two points to remember about the conduction system. We don't have an exit from the normal conduction system near the base. It's closer to the apex, not quite the apex, two thirds, halfway down to the apex. Second is that the conduction system, rather than thinking about it as a right and left bundles, it's a very rapidly branching conduction system with multiple sites getting activated at the same time in both ventricles that allow us to finish ventricular depolarization quickly. And that gives rise to the normal narrow QRS. So this can go wrong in a couple of ways. So one is we have bundle branch block, one bundle is not working. The other side may be perfectly normal, but even if so, the left-sided activation goes from muscle to muscle with wavefront-based propagation than multi-site stimulation at the same time. Makes for a wider QRS. Early part may look okay, but later on gets pretty wide. We could also have basal activation. So normal conduction system waits until you get close to the apex before breaking out, but accessory pathways typically exit near the base. It's muscular activation and produces early abnormal activation. Later parts of the QRS could look normal because by that time, the same beat perhaps has got caught up through the normal conduction system. Now VT by and large is abnormally wide, both abnormalities at the early part of the QRS and later part of the QRS. It starts in muscle, propagates in muscle, and variations where it could be near or originating in the conduction system can produce some confusing morphologies. But by and large, this is the basic construct for why a QRS can be wide during a conducted beat or during tachycardia. So if we've recognized that we're dealing with a wide QRS tachycardia, QRS duration 120, 140, 160, what are the clues that this is VT? The biggest clue is simply playing the odds. Wide QRS VT tachycardias are usually VTs. And the wider the QRS, the more likely it is a VT. So if you have a QRS that's 200 milliseconds and you have a rapid tachycardia, overwhelming odds that you're dealing with VT. The second is just a bit of clinical background. Here I would add questions like, do you know you have heart disease? Have you had a heart attack? Do you have heart failure? And if it's a younger person, fair to ask, have you been told of an abnormal electrocardiogram previously, perhaps already diagnosed with pre-excitation? Once we get through this basics, just understanding wider QRS is likely to be VT and higher chance of VT when there is structural heart disease, we can start focusing on the ECG itself. The simplest I think to scan an ECG for is the axis. It's very difficult with any kind of bundle branch block or most kinds of accessory pathways to have start of activation on the left apical free wall region. So starting there would create an axis that goes to this northwest quadrant. So if you start activation here, producing a northwest axis, you can pretty safely diagnose VT just based on that criteria. And you're comfortable with diagnosing northwest axis simultaneously negative, predominantly negative in lead one and lead AVF, going away from the feet, going away from the left northwest axis VT. The second pure ECG criteria also very useful. And I would say in practice, one of the most common reasons why someone confidently diagnosis VT is you see a relatively regular tachycardia wide QRS, but you can discern P waves, maybe not with every beat, but no discernible relationship with the QRS. So RP, PR intervals varied, even when you can recognize the P waves. So more V than A, no relationship between the A's that you see and the V. This will be VT. We'd all be very comfortable making that diagnosis with extremely rare exceptions. If we look hard enough, you can usually find this in a rhythm strip or a 12-lead ECG about half the time. Either you find the P wave and realize that it's kind of related or unrelated. If you have a longer strip or someone you're able to monitor for a while, I would venture that this is close to 80% of the time, you'll be able to pick this up. The times you won't is when there's underlying AFib, but when there's AFib and a regular tachycardia that's wide QRS, you're pretty sure you're dealing with VT. Concept of fusion beats. So a fusion beat can be for many reasons. It's just a beat that's narrower than expected, presumably because of fusion of two different wavefronts, the origin of the tachycardia and something else. It could be a conducted beat, another PVC, etc. But if you see fusion beats, and the fusion beats are always the beats that come a little earlier, and even better if you can see that there are some P waves that precede the fusion beat, that's VT. So VT is going on. There's probably retrograde block to the atrium. So what you have is sinus beat sneaking down the conduction system every now and then and producing a fused activation sequence in the ventricle. This doesn't happen very often, especially with a limited type of rhythm strip. But if we see for a longer period of time, you can usually pick up one or two fusion beats. The next ECG criteria. So where we're at right now is without memorizing any standard criteria, we've asked the patient about structural heart disease, we've asked the patient about structural heart disease, we've seen how wide the QRS is, remembering wider the QRS, more likely it is VT. We found out whether there's structural heart disease or an abnormal ECG before. We've looked at the axis, we've looked for AV dissociation, we've scanned for fusion beats. And now we come to leveraging the idea, the information that most chest leads drape around the apex. So if we have concordance in the chest leads, if they're all negative, all moving away from the apex, or all positive, all moving towards the apex from the base, and remembering that the normal conduction system tends to exit not quite at the apex, not quite at the base, tells us that bundle branch block, whichever bundle is blocked, cannot produce all positive or all negative on the chest leads. So if it's not bundle branch block, that leaves us VT by far the most common cause of a concordance in the chest leads wide QRS tachycardia. If it's an apical VT, it'll be negative concordance. If it's a basal VT, it'll be positive concordance. Now VT that happens to exit midway will not be concordant. And if there is no concordance, this criteria doesn't help you and make the distinction between a VT and say bundle branch block causing aberrancy during an SVT. Now one important differential diagnosis when there's concordance, all positive, and let's say it's a young person, normal heart, is this could be an accessory pathway. The reason is accessory pathways tend to exit near the base. And if it's an antidromic tachycardia, a tachycardia that's anti-grade conducting down the pathway directly into the ventricular myocardium, you'll get a wide complex tachycardia, positive concordance, indistinguishable from ventricular tachycardia that's arising near the base of the heart. So negative concordance, really only one differential diagnosis, VT. Positive concordance, any clue such as older person, structural heart disease, it'll be VT. But back of your mind, you keep the possibility of a pre-excited tachycardia. Now once we've gotten this far, most of the time you have your diagnosis. And I think this is the key, that before you start looking at details of morphology, you should have a pretty good idea what the diagnosis is. And then in the rare situations where you're unsure, it's good to have a handful of morphological criteria in your pocket to help you a little further. First is bundle branch block is different from wide QRS that sort of looks like a bundle branch block pattern, especially if you have a right bundle-like tachycardia. If you have an initial R and then a true S wave breaks down from the baseline, and then another R wave that's taller, usually about a third to a half, so almost double the height, taller than your initial R wave, that's typical right bundle branch block. And that is a sign of SVT with right bundle aberrancy. But if what you see is just an R wave complex in V1, that has none of those characteristics. There's no S wave here, and the initial R wave is taller. Unless this patient has some complex congenital heart disease, unusual axis, very dilated hearts, just the fact that the right bundle pattern is not typical is enough for you to say that this is SVT. Of course, many of you will recognize this is pretty easy because you do see P waves. There's more QRS than P waves. Several other ways you'd have already diagnosed this, but if those aren't as apparent, this morphological criteria can be applied. Now we talked about the issue that if you have positive concordance or negative concordance, you can say VT most of the time. But what if there isn't? What if there is an RS transition somewhere in the QRS? That means some may be R waves, some may be S waves, but some lead has an RS pattern. So even here, you can use a very simple reasoning and criteria to make the diagnosis. So you look through and see, are there RS complexes? If there are none, it's VT. If there's something that does have an RS complex, then measure from the onset of the R wave, the start of the R wave, to the nadir, not the end, but the lowest point of the S wave. So start of the R to lowest point of the S. And if this is more than 100 milliseconds, this suggests VT. And if it's more than 120, it's almost always VT. So very straightforward approach. Look at the chest leads. Are they all positive? If so, you could have said VT. Are they all negative? If so, you could have said VT. But they're not. Some are positive, some are negative. So we have some leads that have an RS. Every one that you see, an R and an S, measure from the start of the R to the trough or nadir of the S. If any of those that had an RS have this measurement from start of the R to nadir of the S more than 100 milliseconds, it's VT. So remember, measure to the nadir of the S wave. Common mistake is going from either start of the R to the end, that's the whole QRS, or peak to the nadir. Those criteria are not well established. You start from the R to the nadir of the S. So here's an example. Probably not very difficult to make this, but some things are a bit unusual. We have some changes in the morphology, maybe some irregularity, not sure if there's a fusion beat. But we see this RS, start of the R, nadir of the S greater than 100 milliseconds BT. Now, about 10 years ago, there were studies that tried to see, can we use a single lead? And since that time, there have been quite a few that says, just look at a single lead. And a candidate lead is AVR. It's a unique lead because it's in line with the heart. It stares down the barrel of the left ventricle. That means if you're all positive in AVR, you're starting somewhere here, same. It's all positive in AVR is saying essentially northwest axis. If it's negative, we can look a little more carefully to see, can we tell from looking at AVR that's negative to make a guess, is this more likely to be VT or SVT with a balance sheet? And this was the very nice algorithm from Drs. Varecki and Miller. Initial R wave, no brainer, VT. Initial R or Q wave, and even though there is a later S wave, the R wave is either all R or initially R, big R wave, VT. If it's an S that we're seeing, then it could be conduction system, bundle branch block, or could be VT somewhere on the septum near the exit of the conduction system, for example. Then look to see, is there abnormalities in the early part of the QRS, notches, glitches? Notches, glitches means slow conduction, not the conduction system. So slow conduction close to the origin suggests myocardial origin, VT. You could also simply look at the start to the end, the early part versus the later part. If the early part, the later part, most of the time is early, that means near the origin. It's bad conduction, VT. Some kind of classic examples from their paper. This one should be easy, big R wave in AVR. That's the same as saying northwest axis, it's going to be VT. There's an R and an S, but most of the time is that R wave, VT. Now note the SVT patterns. It's never a big positive, but slope is really quick. So early part is nice and smooth rather than these notches or glitches. Look at the preceding ECG when available. All of us will do it. And really, a lot of these skills are when you don't have a baseline ECG for careful comparison. But when there is, if there's WPW and the wide QRS tachycardia has the same axis and overall morphology looks very similar, it's a pre-excited tachycardia. If there is a bundle block, it's a pre-excited tachycardia. It's a bundle branch block that existed, and it looks very similar to the bundle branch block during tachycardia. It's an SVT with bundle branch block. Sometimes it can be tricky, especially with underlying heart disease. Is this all part of the QRS? Are there these P waves? You do have an SRS, but then there's funny looking R prime. Sometimes what you need to do is just observe a little bit longer. And you could see the same pattern, but now with a 2 to 1 tachycardia. Then it's an easy diagnosis. What you had initially was 1 is to 1 conduction. So if we summarize, ask about structural heart disease, look for AV dissociation, and look at the axis. See how wide the QRS is. That will give you the diagnosis. If you need more, look at preceding ECGs, look for concordance. And when there isn't concordance, simple measurement, start of the R to the net year of the S. Occasionally, you'll get something like this, which gives you a lot of information. You'll pick up the start and end of the tachycardia. So when you just look on a rhythm strip here, you could debate this one way or the other, what you're dealing with. But when you look at the start, there's a PAC that starts. First beat of tachycardia, that coupling interval is similar to subsequent beats of tachycardia. When it terminates, you have a sort of intermediate morphology and then narrow beats at the same rate of tachycardia. You'll be sure what you're dealing with here is an SVT with aberrancy. The reverse can also be useful sometimes. This was a patient with a wide complex tachycardia, but not super wide. Suspicion was VT because patient had known structural heart disease. AVR looks positive, but not so wide, seeing some P wave. Could this be a conducted tachycardia with a funny bundle branch block? It could be. And actually, this was a discussion that was going on when the patient presented. But simple maneuver after checking that there's no brewery, carotid sinus massage. Notice what happens. The P waves that we were seeing are getting further away from the QRS and eventually blocking. So there's a retrograde dissociation induced by blocking the AV node, its VT. I will spend about 10 minutes about some patterns of wide QRS tachycardia once you've diagnosed VT that's important in your electrocardiographic and invasive practice. First, outflow pattern. Very, very few people have conduction system that exits in the outflow tract, just a handful over a generation. So if you can recognize outflow pattern, you already know it's VT. And it's specifically outflow VT, benign VT, usually structurally normal heart. What's the outflow pattern? 2,3-AVF are positive, so starting near the head, going to the feet. But uniquely, AVR and AVL are both negative. Our high leads, both negative because we're moving away from the high points of the heart. AVR, AVL negative, 2,3-AVF positive outflow pattern. Very similar from patient to patient. Not always is it benign, though. The caveat is the heart should be normal and you have a regular tachycardia with outflow pattern. This has outflow pattern. But baseline ECG is not normal. Inverted T waves, anterior leads, V1, little bit wider QRS than V5 or V6, maybe can pick up a little notch in V1, epsilon wave. This is right ventricular dysplasia. Another important pattern to recognize. So here, you may have figured out that this is VT using one of the things that we talked about. But this pattern is almost the inverse of the outflow pattern in the sense that it's a left ventricular exit pattern. V1 is positive with a very funny looking bundle branch pattern. But this family of ventricular tachycardias have a very normal looking initial deflection. Look at AVL, very sharp here. AVF, sharp here. 3, sharp here. V1, sharp. Early activation is starting within or close to the conduction system. And these are our conduction system tachycardias. They could be right-sided or left-sided, but usually left-sided. It could be posterior, somewhere in the middle, could be anterior. So the inferior axis can vary, but you'll see this pattern where the initial deflection is relatively sharp. Another pattern recognition ECG. Very regular, very bizarre looking. And it's not only irregular in terms of RR intervals, but each QRS looks different from the other. This should immediately alert you to pre-excited atrial fibrillation. Patient has a pathway, and the patient has developed atrial fibrillation. This is a life-threatening type emergent situation. Patients usually have hemodynamic issues and should be cardioverted. And should be cardioverted to get back to normal rhythm. Few words about wide QRS patterns from less common types of accessory pathways. Common parlance, you'll see this word used, MAHIM, MAHIM fibers, MAHIM tachycardia. Best to understand these as atriofascicular tachycardias or tracts. They connect atrium to the fascicles. They bypass the AV norm. So they're true accessory pathways. But unlike run-of-the-mill pathways that just cross the annulus and exit at the base, they have their own HISS bundle branch-like fiber that can go link up somewhere close to or into the normal conduction system of the heart. Atriofascicular tracts commonly referred to as MAHIM fibers. Contrasted with nodoventricular or nodofascicular tracts, here they are not connecting the atrium to the ventricle or atrium to the fascicle directly. But the wavefront has to go through the AV node or part of the AV node. And instead of that wavefront necessarily going down the HISS bundle, can exit earlier to the base, either to the ventricular myocardium or to a portion of the conduction system. In both atriofascicular tracts and nodofascicular tracts, nodoventricular tracts, you can get tachycardia. Unlike fasciculoventricular tracts, which are a benign variant on the ECG, no tachycardia has come from these. This is just a breach in the insulation of the proximal conduction system. So you can get from the early part of the conduction system to the ventricle rather than needing to wait until you get to the mid or distal ventricle. So a few things that we should look at in terms of terminology with white QRS tachycardias that are related to pathways. Anytime you have a tachycardia where the heart is being activated, the ventricle is being activated through the pathway, antigrade conduction through the pathway, that's a pre-excited tachycardia. So it could be sinus tachycardia, could be atrial tachycardia, atrial flutter, anything. But specifically, if you have conduction down the accessory pathway, a pre-excited tachycardia, but has a retrograde limb that gets back to the atrium, a pre-excited reciprocating tachycardia. This could be retrograde conduction to the AV node, in which case it's called an antedromic tachycardia, down the pathway, up the AV node, or could be a pathway-to-pathway tachycardia. So down one pathway, up through another pathway. It's an example of an ECG of antedromic tachycardia. Would anyone be able to say with certainty, this is not VT? No. All this tells you is concordance, wide QRS, suggests origin near the base of the left ventricle, could be a pathway exiting there, could be a ventricular tachycardia focus there. In the EP lab, we have a very simple maneuver. We just pace the atrium, and you can reproduce almost exactly what that QRS looked like in tachycardia. So even when pre-excitation on the ECG is subtle, in the EP lab, this one step is very helpful. You induce a tachycardia, see what it looks like, pace the atrium faster, see what it looks like. Looks the same. You pretty much know what you're dealing with. Just a few kind of unusual examples to keep in mind. Patient with a grossly abnormal structural heart went on to get a transplant wide QRS tachycardia. We're thinking VT. Induced easily in the EP lab, wide QRS tachycardia, left bundle-ish pattern, very notched, abnormal-looking QRS. Insert catheters, and we note the HISS bundle signal is earlier than either the QRS or atrial activation. Now, if every beat looked like this, we'd be very suspicious of AV node reentry. But it's very wide QRS, and some beats have the HISS, have the V, but no A. The big clue to keep in mind in practice for those situations is get multiple recordings of the HISS, HISS right bundle, early HISS, later HISS. And if that shows an antigrade pattern of activation, this is a conducted tachycardia. Could be AVNRT with block to the atrium on some beats. Could be a HISS bundle or junctional tachycardia. Here you can see that PACs or atrial beats may sometimes change subsequent beats. Other times can be completely dissociated. But we use this clue that the proximal HISS is earlier than the distal HISS, which is earlier than the distal right bundle. Simple maneuver here. A PAC placed from near the AV node can advance the HISS and terminate the tachycardia. This cares about what happens in the atrium near the AV node. This was diagnosed as AVNRT and the slow pathway ablated. Another variant, wide QRS ECG that you should keep in mind. Looks a bit odd. Maybe a hint of a delta wave could easily pass off as a normal ECG. But funny thing that should alert you to the diagnosis is young person with regular tachycardia, but left bundle. Every time there's tachycardia, left bundle morphology. Normal hearts, young people may occasionally get a left bundle branch block aberrancy. But you should be suspicious that what you're dealing with is an atriofascicular tract. Another use of recording HISS and right bundle. Antigrade is HISS before right bundle. Pace the atrium. Produce a wide QRS. Right bundle is earlier than the HISS. You have an atriofascicular tract that's engaging the right bundle in a retrograde manner. And if it completes the circuit, you'll have atriofascicular tachycardia. Can actually find a HISS-like signal away from where we would normally record the HISS. And this would be the signal from where this fiber, the atriofascicular fiber, so-called MAHIM fiber, is located. Last point that I will make about this atriofascicular tracts or fibers is sometimes they can be difficult to see. You may need multi-electrode recordings and careful mapping. But the clue, as an electrophysiologist, would start from the ECG. This is a left bundle pattern. This doesn't show you concordance, so it's not your run-of-the-mill pathway. And it looks similar to bundle branch block. Then you think in a young person, normal heart, anticipate that you may see a fiber in one of these areas. And along the annulus, you search for these HISS-like signals. And that should alert you to where to ablate to get rid of this tachycardia. So to summarize, when you have wide QRS, what do you need to keep in mind as a trainee practicing electrophysiologist? Understand the golden rule of electrocardiography, vector, R-wave, or S-wave. Simple clinical reasoning. Very wide QRS will be VT. Structural heart disease, VT. General rules on the ECG. Northwest axis, VT. V more than A, AV dissociation, V more than A, VT. Fusion beats that come a little early, narrower when early. Maybe you'll see a P-wave before those, VT. Morphology looks. Is it typical bundle branch morphology, especially the right bundle RS, R-prime that's bigger? No, think VT. Concordance. Positive concordance, VT. Negative concordance, VT. No concordance means RS will be present. Look at all the leads within RS. Start of the R to net data of the S. Anything more than 100, VT. Compare previous ECGs when available. Look at the onset. Look at the offset. You'll get additional clues in the difficult case. If you want to look at a single lead, think about AVR. All positive, that's Northwest axis, VT. Mostly positive, VT. Positive or negative, glitches, notches. Useful, especially when you have a QS. Glitches, notches on the descent of that QS in AVR, VT. The early part looks much more abnormal, slurred, taking longer than the distal part, VT. Patterns in VT, outflow pattern, conduction system pattern, accessory pathway pattern, standard pathway, concordant, unusual pathway, atriofascicular pattern and how to use invasive recordings to help you with that diagnosis. And some variants of pathways that you should be familiar with, including the benign fasciculoventricular pattern. Thank you very much for your attention.
Video Summary
In this video, electrophysiologist Dr. Sam Masroudian discusses wide complex tachycardias and how to interpret ECGs to determine if they are ventricular tachycardias (VTs) or supraventricular tachycardias (SVTs) with aberrancy. He explains that understanding the principle of electrical force or vector can help interpret ECG leads and identify positive and negative waves. He also covers the importance of recognizing the location of positive electrodes in different leads.<br /><br />Dr. Masroudian emphasizes that a wide QRS tachycardia is usually a VT, and a wider QRS suggests a greater likelihood of VT. He provides several criteria to help differentiate between VT and SVT with aberrancy, including examining the axis, looking for AV dissociation, and analyzing the morphology of the QRS complexes.<br /><br />He also discusses various patterns of wide complex tachycardias, such as outflow pattern VT, left ventricular exit pattern VT, and pre-excited tachycardias caused by accessory pathways. He explains that recognizing these patterns can aid in diagnosing and differentiating these tachycardias.<br /><br />Lastly, Dr. Masroudian discusses the use of invasive recordings, such as the HISS bundle and right bundle signals, to further confirm the diagnosis of pre-excited tachycardias.<br /><br />In summary, this video provides an in-depth explanation of how to interpret ECGs to differentiate between wide complex tachycardias and highlights various patterns that can help in making a diagnosis.
Keywords
wide complex tachycardias
ECGs
ventricular tachycardias
supraventricular tachycardias
aberrancy
QRS tachycardia
axis
diagnosis
Heart Rhythm Society
1325 G Street NW, Suite 500
Washington, DC 20005
P: 202-464-3400 F: 202-464-3401
E: questions@heartrhythm365.org
© Heart Rhythm Society
Privacy Policy
|
Cookie Declaration
|
Linking Policy
|
Patient Education Disclaimer
|
State Nonprofit Disclosures
|
FAQ
×
Please select your language
1
English