Thursday, February 20, 2020

What are these wide complexes? If unclear by explanation, the laddergram helps to understand.

An 18 y.o. female who presented for chest pain. Patient reports productive cough and headache x 4 days. She notes persistent sternal chest pain worse at night and waking her from sleep. She also notes intermittent abdominal pain, describing as a "tightness".

"Sinus arrhythmia with variable right bundle origin PVCs"
Is this accurate?












No.

This is sinus bradycardia with a slightly accelerated right ventricular escape, such that sometimes:
1.  the sinus beat is conducted before any ventricular escape (beats 7)
2.  the ventricular beat starts at almost the exact same time as the P-wave, and the P-wave therefore does not conduct (beats 6 and 9)
3. the ventricular beat occurs very shortly after the P-wave such that the P-wave does not conduct (beats 2, 3, 5)
4. The ventricular beat fuses to varying degrees with the conducted beat (beats 1, 3, 4, 8)

This is AV dissociation (not NOT AV block).

Her bedside echo was normal and troponins were negative in the ED.

See Dr. Grauer's extensive discussion below for more detail.

This is not pathologic, and not worrisome.

If you see a patient with such a rhythm, simply walk them around on a monitor to increase the sinus rate.  Then the sinus will usurp the ventricular escape and the ECG will normalize at a faster rate.  If not, there is then a problem.

The patient was referred for Holter and it was normal.



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MY Comment by KEN GRAUER, MD (2/20/2020):
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There are LOTS of excellent Learning Points regarding the ECG in this case. For clarity of explanation — I’ve numbered the beats (Figure-1).
  • A QUOTE to Remember  As Rosenbaum said, “Every self-respecting rhythm has at least 3 possible explanations”. There are some details about this interesting arrhythmia that I am not certain of. That said — I don’t think anyone can be absolutely certain of these details without additional monitoring.

Figure-1: The 12-lead ECG and long lead II rhythm strip in this case (See text).



FIRST — I completely agree with Dr. Smith’s interpretation (given above) — regarding the most important clinical points. I’ll add some additional thoughts.
  • For educational purposes — I think the best way to illustrate the Learning Points from this rhythm, is to address the following clinical questions. Please TAKE ANOTHER LOOK at the rhythm in Figure-1, and answer the following:

BASIC Level QUESTIONS:
  • Is there AV dissociation?
  • Is the P-P interval constant?
  • Is there AV block?
  • The patient is an 18-year old woman. Is AIVR (ie, an Accelerated IdioVentricular Rhythm) common in this age group?
  • WHY do the ventricular beats occur in Figure-1?
  • Are there Fusion beats?
  • HOW would you define the rhythm in Figure-1?

ADVANCED Level QUESTIONS: These questions are Beyond-the-Core. The answers to them do not alter management of this patient — but I think the answers are insightful, and help to hone your ECG interpretation skills beyond the basic level.
  • Are all P waves in the rhythm in Figure-1 the same?
  • Is this really a sinus rhythm?
  • WHICH are the fusion beats in Figure-1Do we really know HOW MANY fusion beats there are?
  • WHY does QRS morphology of the conducted beats (ie, beats #1,4,7,8) change?

HINT: If you do not use calipers — You will not be able to answer many of the above questions ...



Ithere ADissociation? — By definition, there is transient AV dissociation in Figure-1. That’s because, at least for some brief period of time — there are some P waves that are not related to neighboring QRS complexes!
  • I’ve labeled P waves in the long lead II rhythm strip in Figure-2 (BLUE arrows). It looks like beats #1,4,7 and 8 are conducting — because they are all preceded by P waves with a constant and normal PR interval.
  • Since the PR interval preceding beats #2,3,5,6 and 9 is clearly much shorter than the PR interval of conducted beats — this means that beats #2,3,5,6 and 9 are not normally conducted. Therefore — there is AV dissociation for these beats!
  • For more on AV Dissociation — CLICK HERE.

Figure-2: P waves in the long lead II rhythm strip have been labeled with BLUE arrows (See text).



Ithe P-P Interval Constant? — Careful observation of the BLUE arrows in Figure-2 should tell you that the P-P interval is not constant. (IF in doubt — calipers will confirm this for you in 2-3 seconds).
  • At the least — there is sinus arrhythmia ...

Ithere ABlock? — There is no evidence of AV block in Figure-2. That’s because although some of the P waves in this rhythm strip are not conducting — P waves never have a chance to conduct, because the PR interval preceding beats #2,3,5,6 and 9 is clearly too short to allow normal conduction.
  • PEARL #1  Remember that there are potential Causes of ADissociation: i) AV dissociation due to some form of 2nd or 3rd degree AV Blockii) AV dissociation by Usurpation” — in which P waves transiently do not conduct because an accelerated junctional or ventricular rhythm takes over the pacemaking function (because it is faster than the underlying sinus rhythm); and/oriii) AV dissociation by Default” — in which a junctional or ventricular escape rhythm takes over by “default” (ie, because of SA node slowing).

IAIVR Common in an 18yo? — The ventricular beats in Figure-2 are beats #2, 3, 5, 6 and 9. The usual idioventricular escape rate in adults is between 20-40/minute. As per Dr. Smith — since the rate of the ventricular beats in this case is slightly faster than this (ie, ~55-60/minute) — this is a slightly accelerated ventricular rhythm ( = AIVR).
  • For brief review of AIVR — CLICK HERE. The common Clinical Settings in which AIVR may occur include: ias a rhythm during cardiac arrest; ii) in the monitoring phase of acute MI (especially with inferior MI); oriii) as a reperfusion arrhythmia (following thrombolysis, acute angioplasty, or spontaneous reperfusion). AIVR may also occur in patients with underlying coronary disease, cardiomyopathy, and with digoxin toxicity.
  • PEARL #2  On rare occasions, AIVR may occur intermittently in otherwise healthy subjects without underlying heart disease. In such cases — this rhythm is often associated with increased vagal tone. If these individuals are asymptomatic — the rhythm is generally benign, and no treatment is needed. Assuming the Echo is normal for the 18yo woman in this case — and provided that the “chest pain” reported by this patient is not related to the rhythm we see in Figure-2 — no additional evaluation would be needed.

Figure-3: I’ve measured R-R intervals in milliseconds in the long lead II rhythm strip (See text).



WHY do the Ventricular Beats Occur? — To assist in answering this question — I have carefully measured the R-R intervals in the long lead II rhythm strip (Figure-3).
  • PEARL #3  When confronted with a rhythm strip in which there is transient AV dissociation, and you are not certain as to which beat(s) may be conducting — Look for unexpected shortening of the R-R interval. Such shortening usually indicates which beat(s) is being conducted. Conversely — lengthening of the R-R interval often tells you which beat(s) originate from another focus.
  • Beat #4 in Figure-3 is preceded by the shortest R-R interval (865 msec) — and we know this beat is conducting.
  • The next shortest R-R intervals in Figure-3 precede beats #7 and 8 (1045 msec) — which we know are both conducted by the P waves that precede them.
  • The reason all other beats (ie, beats #2,3,5,6 and 9) are at least in part ventricular beats — is that they are all preceded by longer R-R intervals. It is because the appearance of P waves is delayed — that the slightly accelerated ventricular focus “gets tired of waiting”, and puts out a ventricular beat.

Are there Fusion Beats? — To assist in answering this question — I have drawn a Laddergram of the rhythm (Figure-4).
  • PEARL #4  Although becoming comfortable in drawing laddergrams takes time (it literally took me a few decades to get good at this skill!) — learning to read laddergrams is EASY, and takes no more than a few minutes. (IF interested in some user-friendly examples to get you started — CLICK HERE — and HERE — and HERE).
  • P waves precede each of the 9 beats in the long lead II rhythm strip in Figure-4. Isn’t it now much easier to see the irregularity in the P-P interval looking at the Atrial (upper level) tier?
  • Beats #1,4,7 and 8 are conducting.
  • I’ve drawn RED circles at the bottom of the laddergram that represent ventricular origin for beats #2,3,5,6 and 9.
  • My educated guess is that the P waves preceding beats #6 and 9 occur too soon before these ventricular beats to be conducted.
  • On the other hand — the PR interval preceding beats #2,3 and 5 is a little longer than that preceding beats #6 and 9 — such that there may have been time for some conduction from above to have occurred. Although hard to tell — the QRS of beats #2,3 and 5 appears to be a little smaller and narrower than that for beats #6 and 9 — so beats #2,3 and 5 appear to be Fusion beats (schematically represented in the laddergram by simultaneous conduction into the Ventricular tier from above and below).
  • For more on Fusion beats — CLICK HERE.

Figure-4: Laddergram of the long lead II rhythm strip (See text).



WHAT is the Rhythm? — The answer to this question leads us to PEARL #5: The term “AV Dissociation” should never be used as a “diagnosis” per se. Instead — optimal rhythm interpretation indicates there is AV dissociation because of which one or two of the 3 potential causes of AV dissociation discussed in PEARL #1 are operative.
  • The primary problem in the rhythm shown in Figure-4 is bradycardia. It is because of sinus bradycardia and arrhythmia that AV dissociation is seen, with several beats from a slightly accelerated ventricular focus.
  • Thus, the rhythm is not “AV dissociation”. Instead — we see AV dissociation bdefault of the sinus pacemaker that slows enough to allow the slightly accelerated ventricular focus to put out several ventricular beats. NOTE: Semantically — this is not pure AV dissociation by “default” — since rather than simple ventricular “escape” — the ventricular focus is faster than the 20-40/minute rate of a ventricular escape rhythm.


ANSWERS to the ADVANCED Questions: Earlier — I posed the following Beyond-the-Core questions.
  • Are all P waves in the rhythm the same?
  • Is this really a sinus rhythm?
  • WHICH are the fusion beats in the rhythm? Do we really know HOW MANY fusion beats there are?
  • WHY does QRS morphology of the conducted beats (ie, beats #1,4,7,8) change?

Figure-5: I’ve labeled all P waves with letters (See text).



MANSWERS:
  • I believe that P wave morphology is not the same for all of the P waves in Figure-5! Although it is true that there will always be some slight “natural” variation in P wave morphology — DON’T YOU THINK that P waves a,c,d and g are clearly more pointed than P waves e,f and i? (I’m not sure about b, which seems to manifest an in-between morphology).
  • IF in doubt — GO BACK to the 12-lead tracing in Figure-1, and look at P wave morphology in all 12 leads. I believe there are some subtle differences that are real.
  • Note that the rounder P waves (ie, e,f and i) seem to be preceded by a somewhat longer R-R interval. Clinically — I suspect that rather than sinus arrhythmia, this 18yo probably has a wandering atrial pacemaker — with the marked variation in P-P interval (as well as her AIVR) all being manifestations of increased baseline vagal tone. Shift in the site of the atrial pacemaker may be occurring with ongoing variation in vagal tone. That said — to know for certain if the rhythm was a wandering pacer, we'd need a longer period of monitoring — and we'd need to be sure we were seeing at least 3 different P wave morphologies (For more on ECG diagnosis of wandering pacemaker — CLICK HERE).
  • Note that we never see a ventricular beat not preceded by any P wave in Figure-5. As a result — we have NO idea as to what a “pure” ventricular beat looks like. It is therefore possible that even beats #6 and 9 might manifest a slight degree of fusion (ie, we have NO idea as to how many fusion beats we are seeing in this rhythm strip).
  • Finally — Note that the S wave of the earliest conducted beat (ie, beat #4) is slightly wider than the S wave of conducted beats #7 and 8. I do not think beat #4 is a fusion beat — because the PR interval is identical to that of other conducted beats, and it is only the terminal S wave that looks slightly wider. Instead — earlier occurrence of beat #4 is probably the result of some incomplete RBBB aberration.

BOTTOM LINE  Assuming this 18yo has no underlying structural heart disease — her interesting rhythm is almost certainly benign. There are no acute ST-T wave changes on conducted beats in her 12-lead tracing.
  • My hope is that attention to some of the above "picky" details in complex rhythm interpretation are insightful.

Our THANKS to Dr. Smith for presenting this case!


11 comments:

  1. A detailed and comprehensive analysis, as usual. I would just make one minor point – I think that beat #7 is also a fusion beat, albeit mostly conducted, because of the depth and narrowness of the S wave compared to those of beats 1, 4 and 7.

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    1. Hi Dave! THANKS for your comment! As per my explanation above — I thought it more likely that we were seeing variations of some incomplete RBBB aberrant conduction (which would uniquely alter only the last portion of the QRS deflection) — given what looks like identical PR intervals preceding conducted beats # 1, 4, 7 and 8 + identical QRS deflections for all but the terminal portion of ventricular depolarization. Then again — P wave morphology preceding conducted beats #1, 4 and 7 ( = pointed P waves) IS a bit different than P wave morphology preceding beat #8 ( = a smaller P, and a bit rounder) — so impossible to be certain what a “conducting PR interval” would be for this P in front of beat #8 (compared to the P in front of beat #7 — if this P wave is from another atrial site in association with a wandering atrial pacemaker …). And as I acknowledge, since we NEVER see a ventricular beat not preceded by a P wave — we don’t know what a “pure” ventricular beat QRS complex would look like — so impossible to know for certain how many fusion beats we truly have. You could be right about beat #7 … — and perhaps I could be right. That’s why I fully acknowledged that I was NOT certain about some details — and why I started My Comment with Rosenbaum’s quote that “Every self-respecting rhythm has at least 3 possible explanations”. THANKS again — I ALWAYS enjoy reading your comments on complex arrhythmias! — :)

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  2. Thank you for your scientific and detailed interpretation. I have another explenation for QRS morphology change. R-R interval in wide QRS beats are longer than narrow beats. It can be explained by phase 4 block in left bundle branch (bradycardia dependent aberrancy). I know that this pattern is usually seen in abnormal hearts, but EPS and H-V interval can differentiate between ventricular origin of wide beats vs. Junctional beats with aberrancy due to phase 4 block mechanism. Thanks again for your comprehensive explenation.

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    1. Thanks for your comment! Yes, it could be possible that there is Phase 4 block (ie, bradycardia-related BBB) as the cause of the wide beats. That said — my hunch is that this is NOT the mechanism for the wide beats in Figure-4 because: i) there are fusion beats; ii) QRS morphology (as shown in the 12-lead in my Figure-1) is very ATYPICAL for LBBB aberration because of the lack of a monophasic R wave in lead V6 (One would expect rate-related aberrant conduction in an otherwise healthy young adult to manifest a more typical form of either RBBB or LBBB); iii) QRS morphology is not-at-all like RBBB (and in otherwise healthy young adults, the right bundle branch tends to have a longer refractory period — therefore it being much more likely than aberrant conduction [include Phase 4 block] will manifest an RBBB pattern); and iv) in “real life” — Phase 4 block is extremely uncommon (if not rare) — though YES, I have seen cases of this. BOTTOM LINE: “Never say never” — but ( = my opinion) — I’m skeptical that this is Phase 4 block — :)

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  3. Thanks for a detailed explanation. My question about AV dissociation: Is it correct to say the amplitude of the complexes will vary depending if p waves are conducted or non conducted?

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    1. @ Polly — Thanks for your question. There are several ways that QRS complexes may vary in shape (and/or amplitude) when there is AV dissociation. IF a P wave is not at all conducted — then there will be either an escape or accelerated “subsidiary” pacemaker (coming either from the AV node, the His, a fascicle, or the ventricles) — and the QRS complex will reflect that shape. IF the escape (or accelerated) pacemaker is from the AV node — then the QRS complex may look very much like (possibly even identical) to sinus-conducted beats. And then if there is FUSION — in this case the QRS will look “in between” the shape of the conducted beats and the shape of that other pacemaker. Depending on “how much fusion” takes place — the shape of the QRS complex will look either more or less like the sinus-conducted beats (vs the other focus beats). I explain and illustrate all of this in the LINK that I provide above re “More on Fusion Beats”. SORRY for the “involved” answer — but it REALLY DEPENDS on the specific tracing you are looking at … If you have specific questions regarding my laddergram ( = my Figure-4 above) — the beats are numbered — so let me know which beat you are wondering about. Hope the above explanation is helpful to you — :)

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  4. Ken...

    I would have responded earlier but I'm writing this from Reykjavik. That was an exellent analysis! Of course, I have a few things to add (if I may)...

    I think the basis of the ventricular dysrhythmia is a ventricular parasystole. While it can act as an AIVR, they aren't exactly the same thing. However, I would have no argument if someone said it is one cause of AIVR - it just boils down to a nuance of definition. Two sets of successive ventricular ectopic beats are 1055 and 1060. The difference is trivial since exit blocks/delays can cause such variations. The ventricular ectopics seem to pick up right on time after having been interrupted by the sinus rhythm, which suggests some degree of "protection" due to entry block indicative of ventricular parasystole. This "protection" is neither absolute nor magic. It really all depends on the timing of the parasystolic and sinus-conducted beats. However, this still fits in with everything you said about the ventricular rhythm.

    The atrial rhythm is also very ionteresting on its own. This is a an otherwise healthy teenage female. She certainly could have a significant degree of sinus arrhythmia (and likely does!). The first 3 P waves appear similar enough to me to call them sinus. The 4th P wave appears disproportionately early to be part of the gradual wax and wane of sinus arrhythmia PLUS its morphology is very visibly different - sharply peaked. This ia a PAC that comes early enough to conduct to the ventricles normally, thus usurping the ventricular parasystolic focus for one beat. The 4th P wave has now resulted in a compensatory pause (for newbies, whether a pause is compensatory or not depends on the P-P interval - NOT the R-R interval). Now look at the P wave that ends this pause (#5) - it is, once again, completely different than the sinus P wave and the ectopic P' wave. This P wave is very rounded, almost like a semi-circle. It also terminates the longest P-P interval: this is an atrial escape beat. What fascinates me most about this beat is that atrial escapes are rather rare (at least the ones we can differentiate!)! Beat 6 is probably also an atrial escape (though it COULD be sinus). There is a longer P-P interval at the end of the strip which is probably also terminated by an atrial escape.

    One more comment about capture beats - the PR interval of the capture beat may be prolonged (it does NOT have to have a "normal" PR interval) and the resulting QRS may conduct with some aberrancy. The significant finding is that there is a QRS ending a short R-R interval.

    So many people struggle with the distinction between AV dissociation caused by 3rd degree AV block and simple AV dissociation. All you have to do is look at the R-R intervals. If you find one is shorter than the rest, then you have AV conduction and no block.

    This tracing exhibited AV dissociation by usurpation in the ventricles but also sino-atrial dissociation by default in the right atrium.

    This is a fascinating rhythm strip! Thanks again!

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    1. Hi Jerry. THANKS for your Comments — all the way from Iceland !!! Your thoughts (and those above of David Richley, who like yourself is an arrhythmia connoisseur) are the very reason I began My Comment citing Rosenbaum, “Every self-respecting rhythm has at least 3 possible explanations”. I always appreciate your insights — though I don’t agree in this case … — but then again (as per Rosenbaum) — I cannot say that you, or Dave or I is the one who is correct … Reasons I don’t think this is ventricular parasystole are: i) True ventricular parasystole is extremely uncommon, especially in a young adult (NOT impossible, but in my experience of looking for parasystole over decades — I just don’t see it much); and ii) The R-R interval between beats #2-3 = 1055 msec — whereas the R-R interval between beats #3-5 = 865 + 1075 = 1940 (which is 170 msec shorter than the expected value of 1055 X 2 = 2110 msec if there was 2:1 Exit Block). Of course, interectopic intervals are never perfectly geometric — but this amount is more than I would expect for an interectopic interval right next to beats #2 and 3 — whereas the R-R interval preceding beat #5 (1075 msec) IS just about what I’d expect for the slightly accelerated idioventricular pacemaker in this case that is responding to the brief pause after beat #4. All of that said — as you know — it’s impossible to diagnose parasystole from a single short tracing without confirmation that interectopic intervals truly repeat over time …

      Otherwise — we once again need a longer period of monitoring regarding the atrial rhythm in order to flesh out if the slight variation in P wave morphology of the 2nd P wave ( b in my Figure-5) is “real” vs pointed and similar to P waves labeled a, c, d, g. But I think it is perfectly reasonable to postulate sinus bradycardia arrhythmia, with shift of the atrial pacemaker for the atrial rhythm. I don’t think the 4th P wave (d) is sufficiently premature to have to be a PAC — but rather could reflect sinus arrhythmia in this young adult who I suspect has increased vagal tone. OF COURSE — I can’t prove any of this — and as I state above, you and/or Dave could be right, and I could be wrong. That’s the FUN of discussing complex arrhythmias — so that this case holds a LOT of interesting material BOTH for clinicians less “into” complex arrhythmia mechanisms (who still NEED to be able to recognize the underlying bradycardia with AV dissociation and ventricular beats + the absence of any AV block!) — as well as for folks like you, myself & Dave who postulate on the above subtleties. THANKS again for your thoughts! — :)

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    2. Thanks, Ken...

      I certainly agree that there is more than one way to interpret an ECG or even a rhythm strip. Marriott (and others) occasionally presented more than one laddergram for a single dysrhythmia. I have difficulty with an otherwise healthy 18 year old developing an AIVR, which I find no less unusual than a ventricular parasystole. Parasystolic foci are affected by the refractoriness of the tissue around each focus which can result in a delayed exit or no exit at all. A much longer rhythm strip would certainly have been helpful. Most cardiologists and EPs that specialize in parasysole allow a variance of 0.08 to 0.12 seconds for the beats due to exit delay and block. Parasytolic foci are also susceptible to Mobitz I and Mobitz II blocks.

      Unfortunately, none of this is really settled by this tracing. I just hope that it stimulates more people with interest in electrocardiography to realize that there is a lot more to learn and they are capable of learning it.

      I still stand by my interpretation of the atrial rhythm but all three of us could change our minds with a longer rhythm strip. One point that remains, however, is that all three of our interpretations would likely result in exactly the same approach to treatment. There is certainly no argument about what we see there - just the origin behind what we see.

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