Thursday, January 31, 2019

What is the Rhythm?

----------------------------------------------------
Presentation by KEN GRAUER, MD:
----------------------------------------------------
The Case: A previously healthy young man presented to the ED for shortness of breath and chest pressure that occurred ~3 hours earlier, when he suddenly felt his heart “skip a beat”, and then begin “racing”. He felt “lightheaded” (presyncopal) during the episode — with the “strong sensation of his heart beating”. He did not feel better until ~45 minutes later. Similar episodes had occurred over the past month — but none lasted as long.  Of note, the patient is an active athlete. There is a family history of a “junctional or other abnormal rhythm”.

Figure-1 shows his initial ECG that was obtained in the ED.

Hint:
  • Use of calipers is strongly advised for interpreting the rhythm!
Figure-1: The initial ECG in this case (See text). 

Questions:
  • What is the rhythm in Figure-1?
  • Why is this not, strictly speaking, “isorhythmic” AV dissociation?
  • Might the family history of an abnormal rhythm have anything to do with this case?
  • Clinically — What would you do for this patient?
==========================
PEARL #1: The easiest way to instantly enhance your arrhythmia interpretation skills is by using CALIPERS. The cardiologist who does not regularly use calipers for interpretation of complex arrhythmias — is a cardiologist who will miss the diagnosis on more than a few occasions.
  • Obviously, not all arrhythmias are amenable to use of calipers. You’ll often know the etiology of a particular rhythm without the need for calipers. And, in an acute emergency situation — there is often no time to stop and pull out calipers until you’ve taken care of the patient. That said, calipers instantly make you smarter. They excel for assessment of AV blocks and AV dissociation — they allow instant determination if a rhythm is or is not regular — and, calipers are invaluable for deducing whether or not various beats are being conducted.
  • Using calipers will NOT slow you down. On the contrary — with a little bit of practice, you’ll find they dramatically speed up the interpretation of many complex arrhythmias — because you can instantly measure and compare intervals.
PEARL #2: When discussing a complex rhythm — Numbering the beats is of invaluable assistance for clarifying which beat is being referred to (Figure-2).
Figure-2: We have numbered the beats in the long lead II rhythm strip at the bottom of the tracing (See text).
==========================
Initial Assessment of the Rhythm: When confronted with a complex arrhythmia — I always like to begin with WHAT I KNOW to be true.
  • I know that the PR interval in front of beat #6 is too short to conduct. The PR interval in front of beat #2 is also too short to conduct. This suggests that there is at least transient AV dissociation — which simply means that there are sinus P waves present that are not related to neighboring QRS complexes.
  • The longest PR interval in Figure-2 appears before beats #8 and 9. The PR interval preceding these 2 beats is equal and normal — and the P wave in this lead II is upright. This suggests that beats #8 and 9 are most probably sinus-conducted.
  • There seems to be indication of LOTS of P waves on this long lead II rhythm strip. PEARL #3: Clarification of a complex rhythm is often much EASIER to attain IF you are able to label underlying atrial activity. We do so in Figure-3.
Figure-3: RED arrows indicate what we believe is the underlying atrial rhythm (See text). 
==========================
Assessment of Figure-3: Although some of the P waves highlighted by RED arrows in Figure-3 are partially hidden by neighboring QRS complexes — overall P wave morphology appears to be the same throughout this tracing. Therefore, there is an underlying sinus mechanism.
  • BUT — the P-P interval of these RED arrows varies throughout the tracing! This tells us that the underlying rhythm is a fairly marked sinus arrhythmia. It should be emphasized that of itself — sinus arrhythmia is not an abnormal rhythm in an otherwise healthy young adult.
  • All 10 QRS complexes in this tracing are narrow. These QRS complexes all look similar — although there are slight differences in QRS morphology for some of the beats. But the fact that there are some sinus-conducted beats — as well as many other beats with PR intervals that are definitely too short to conduct — tells us that there are junctional escape beats (ie, beats #3, 4, 5 and 6 at least — are all junctional beats).
==========================
Putting Together What WKnow Thus Far: The underlying rhythm is sinus bradycardia with marked sinus arrhythmia. As a result of slowing of the sinus pacemaker — the sinus rate occasionally drops below the intrinsic rate of the AV nodal escape pacemaker. This results in transient AV dissociation — until the sinus node speeds up enough to exceed the intrinsic AV nodal escape rate. This phenomenon is best known as, ADissociation by “Default” — ie, “default” of the sinus pacemaker due to marked sinus bradycardia, which transiently allows the AV nodal escape pacemaker to take over. We emphasize the following KEY points:
  • The rhythm in Figure-3 is not “AV dissociation”. AV dissociation is never the etiology of a rhythm. Instead, as we state above — the rhythm is sinus bradycardia with marked sinus arrhythmia. It is because of marked slowing in the rate that AV dissociation arises.
  • There is absolutely no evidence of any form of AV block. This is because we never see any P waves that fail to conduct despite adequate opportunity to conduct! Instead, the reason why certain P waves do not conduct — is simply that the PR interval is too short.
  • This is not “isorhythmic” AV dissociation. The word “iso” — is from the Greek word “isos” — which means “equal”. True isorhythmic” AV dissociation is an uncommon phenomenon, in which there are independent atrial and ventricular pacemakers that are beating at nearly identical (ie, “equal” ) rates. Most often, there is an underlying sinus (atrial ) rhythm competing with an AV nodal rhythm beating at an almost identical rate. The effect is like a horse race — in which one rhythm temporarily “takes the lead” (ie, takes over the rhythm) — until it either slows slightly, or until the other rhythm accelerates just enough to take over the rhythm — and then this back-and-forth process begins anew. This is not what we see in Figure-3 — as there is an obvious marked difference in P-P and R-R intervals for much of the long lead II rhythm strip.
==========================
NOTE — It is important to appreciate that there are 3 potential Causes of ADissociation:
  • AV dissociation due to some form of 2nd or 3rd degree AV Block;
  • AV dissociation by “Usurpation” — in which P waves transiently do not conduct because an accelerated junctional rhythm takes over the pacemaking function (because it is faster than the underlying sinus rhythm); and/or,
  • AV dissociation by Default” — in which a junctional escape rhythm takes over by “default” (ie, because of SA node slowing — as occurs in this case).
==========================
But there is MORE to this case … (WARNING: What follows involves advanced arrhythmia concepts! ).

Question:
  • What is atypical about the rhythm in the long lead II of Figure-3, compared to what we most often see when there are junctional escape beats?
Hint:
  • The answer is revealed in Figure-4, in which careful caliper measurement provides the duration of all P-P intervals (in PURPLE lettering) — and the duration of the R-R interval preceding each of the first 6 beats (in BLUE lettering). What do you see?
Figure-4: We have carefully measured the number of large boxes for the critical intervals illustrated above (See text). 
==========================
Assessment of Figure-4: Most of the time, the intrinsic rate of the escape junctional pacemaker is constant. We are generally able to use this finding to help determine which beats are junctional vs conducted — because the R-R interval preceding most beats in a junctional escape rhythm is the same. But this is not the case in Figure-4 — because despite our thought that beats #2-thru-6 are all junctional escape beats (since they are all preceded by a PR interval too short to conduct) — the preceding R-R interval varies from 4.8-to-5.1 large boxes.
  • PEARL #4: The QRS complex of junctional escape beats sometimes looks a little bit different than the QRS of sinus-conducted beats. The reason is that the path of the electrical impulse for a sinus beat — may differ slightly from the path of a junctional beat that begins lower down or more to one side or the other of the AV node. We see this in Figure-4. We know beats #8 and 9 are sinus-conducted. We see a small-but-definitely-present initial q wave in these beats that is not seen in junctional beats #3, 4, 5 and 6. In addition, R wave amplitude of junctional beats #4 and 5 is clearly taller than the R wave of sinus-conducted beats #8 and 9! This PEARL is sometimes invaluable for telling us which beats in a tracing with AV dissociation are sinus-conducted vs of junctional origin vs fusion beats.
  • Then WHY does the QRS complex of beat #10 look exactly like the QRS of sinus-conducted beats #8 and 9, despite being preceded by a shorter PR interval? I believe the answer is that this patient manifests a component of Vagotonic AV Block (albeit not yet with clear demonstration of AV block ... ).
==========================
I discuss in detail the phenomenon of Vagotonic ABlock in THIS CASE. In the interest of brevity here — Suffice it to say that some otherwise completely healthy individuals manifest a marked increase in vagal tone, to the point that significant bradycardia with various forms of AV block may sometimes be seen despite complete absence of underlying structural heart disease. Among the characteristics of this syndrome are marked sinus arrhythmia, variation in the rate of escape pacemakers, variable PR intervals for sinus-conducted beats (that is otherwise hard to explain) — and at times, various forms of transient AV block.
  • Returning to Figure-4 — I believe the fact that the QRS complex of beat #10 is identical to the QRS of known sinus-conducted beats #8 and 9 — tells us that beat #10 is most probably sinus-conducted with a slightly shorter PR interval. The same is likely to be true for beats #1 and 7 — each of which is preceded by a PR interval slightly shorter than the PR interval of known sinus-conducted beats #8 and 9. It’s hard to know about beat #2 (the QRS looks like a sinus-conducted beat — but the PR interval is exceedingly short ... ). But overall, considering variation in the R-R intervals preceding known junctional escape beats #3, 4, 5 and 6 — the composite of findings suggest profound vagal influence affecting this patient!
  • The fact that there is a family history of some "abnormal" rhythm — suggests there may be a familial component to this patient’s inherently increased vagal tone.
  • Finally — this patient’s symptoms almost seem out of proportion to the rhythm we see in Figure-4. After all, there are no runs of tachycardia, no profound bradycardia, and as yet no sign of AV block. Close follow-up is essential. Holter monitoring may well reveal other more worrisome arrhythmias over the course of a day. That said, even though vagotonic AV block most often has a benign prognosis — the fact that this patient is so symptomatic (with what sounds like presyncope) merits referral to an EP cardiologist for more thorough evaluation and risk assessment.
BOTTOM LINE — Complete explanation of all findings present in the ECG shown in this case is indeed complex! I would be ecstatic for anyone assessing the rhythm in Figure-1 as showing marked sinus bradycardia and arrhythmia, that sometimes results in sufficient sinus slowing to produce AV dissociation with junctional escape beats. I think it important to appreciate that there is no evidence of AV block in Figure-1. That said — I think it helpful to be aware of the phenomenon of vagotonic AV block, that although uncommon — will be seen from time-to-time by emergency providers (Review of THIS CASE may prove insightful). In this particular case, even though AV block is not seen in Figure-1 — there are a number of ECG findings that in the context of the significant symptoms experienced by this patient, point to an inherent increase in vagal tone that merits referral for more complete assessment.

==========================
For More Info:
  • For another example of my step-by-step approach to assessing a case of AV dissociation — CLICK HERE
  • For those wanting a VIDEO Review (58 minutes) of the ECG Diagnosis of AV Blocks & AV Dissociation CLICK HERE. If you click on SHOW MORE (under the video on the YouTube page) — you’ll see a linked Contents of all that is covered in the video. The part regarding AV Dissociation BEGINS HERE.

21 comments:

  1. An interesting tracing where vagal tone and the act of respiration are affecting sinus rate with slight sinus arrhythmia, even intrinsic junctional rate slightly, QRS height and PR interval. The sinus rate slows just enough to allow junctional escape to occur, resulting the sinus P wave and the junctional QRS to occur close together during each other's physiologic refractory period, resulting in an obligatory AV dissociation, a physiologic phenomenon. If the sinus beat occur early enough, it has no problem conduction (capture beats), which proves that there is no AV block. I said the act of respiration is affecting the sinus rate and the QRS height, i.e. when the sinus rate speeds up with inspiration, that is when the QRS height shortens due to the inflated lungs buffering the heart(see beats 7,8,and 9 of the rhythm strip of lead II.)
    K. Wang.

    ReplyDelete
    Replies
    1. THANKS so much K for your comment. My thought had been that the reason for change in QRS appearance (slightly taller R waves and loss of the small initial q wave) for beats #3,4,5 and 6 — was that these were junctional beats — whereas beats #1,7, 8, 9 and 10 were sinus-conducted (some with a shorter PR interval). This left me with beat #2 about which I was less certain — as the QRS of beat #2 seem to suggest a sinus-conducted beat — but the PR interval looked too short ... In my experience, on occasion AV nodal beats will look just a little different than sinus-conducted beats — and this relationship can then be VERY helpful for determining if a certain beat is being conducted or is junctional escape. THANKS again for your informative comment!

      Delete
    2. Q waves are "gone" in beats 3,4,5 and 6 because the P wave is there.
      K. Wang.

      Delete
    3. And beat 2 is junctional( the PR is too short).
      K. Wang.

      Delete
    4. Regarding "Q waves gone" = Maybe — but how ‘bout beat #4? And for beat #6 in which the peak of the P is gone before the onset of the QRS, shouldn’t there then be some negative deflection at the onset of the QRS? And to me, the R wave is clearly taller for the junctional beats … I wish we had a longer period of monitoring to settle these issues. THANKS again so much K for your comments, which are ALWAYS tremendously insightful! — :)

      Delete
    5. You elegantly identified P waves with red arrows. I this patient, the base of the P wave is about 120ms wide, the QRS is 100ms wide. The P wave is clearly in front of R1, barely in front in R2, R3 occurs within the P wave, P and R4 began together, R5 within the P and the P wave is barely in front of R6. So, "Q waves are gone" because they are superimposed with P waves definitely, not maybe. Of course, slightly different parts of the P wave.
      K. Wang.

      Delete
  2. Good one.
    With the transient AV dissociation, I initially thought it was a short run of fascicular VT.

    ReplyDelete
    Replies
    1. Against your theory is no more than minimal change in QRS morphology (No QRS widening) as the rate speeds up ...

      Delete
  3. Excellent and full of knowledge case. Thank you very much Dr.Ken Grauer and Dr.K Wang for the iformative comments.

    Few years back, there were video lessons from Dr.Grauer and also Dr.K Wang and Dr.Smith( on this blog) on
    regular basis which were really informative . Hope the trend continues again.

    ReplyDelete
  4. Excellent and full of knowledge case. Thank you very much Dr.Ken Grauer and Dr.K Wang for the iformative comments.

    Few years back, there were video lessons from Dr.Grauer and also Dr.K Wang and Dr.Smith( on this blog) on
    regular basis which were really informative . Hope the trend continues again.

    ReplyDelete
    Replies
    1. @ Unknown — The ECG videos that I have made are available at http://www.videoecg.com — Demands on my time prevent me from making more ... THANKS again for your kind words! — :)

      Delete
  5. Ken…

    Part I

    This is a really GREAT teaching ECG and there is a huge amount to learn from it. I enjoyed Dr. K.Wang’s remarks also. If you just sit back and take in the overall picture of this rhythm strip, you can see the cyclical nature of the changes in R wave amplitude that follow a respiratory-type rhythm pattern. In addition to the buffering of the QRS voltage by the expanded lungs, there is also diaphragmatic motion that may be causing a bit of axis shift as well.

    While I certainly agree with you on most points, I do have a different take on others. First, let me say “Thank you!” for emphasizing the use of calipers in ECG interpretation. They are useful in so many ways. I include a set of calipers for every participant in my advanced ECG courses plus I take the time to show them how to use them in specific situations.

    First, I think one is going down a dangerous path in using the PR interval and P wave morphology to determine whether or not a sinus P wave has conducted in the setting of an obvious AV dissociation. In such cases, a “normal” PR interval has little meaning if the ectopic pacemaker rhythm remains regular. In fact, even those P waves that DO manage to conduct and produce escape beats often have PR intervals that are longer than whatever is “normal” for that patient. Just from this ECG, we really have no idea what this man’s typical PR interval is under more normal conditions. If his “normal” PR interval were 0.26 seconds under regular circumstances, then the “normal” PR intervals for beats 8 and 9 most assuredly did NOT conduct. There are two types of “normal” PR intervals – the statistically “normal” intervals from 0.12 – 0.20 seconds but also whatever happens to be “normal” for that particular patient. While we can generally assume that a PR interval less than 0.12 seconds most likely did NOT conduct, we can’t ALWAYS assume that a PR interval of 0.18 seconds actually DID conduct. It all depends on the “normal” PR interval for that patient.

    (continued in next post – Part II)

    ReplyDelete
  6. Part II

    Another issue is the sudden change in the H’-H’ intervals (for any newbies, H’ refers to an ectopic junctional beat). From the first beat to the seventh beat we see a gradual increase in the sinus rate (inspiration is occurring here). Let’s look at the 7th and the 8th beats. While the 8th P-QRS is very obviously early (it doesn’t take calipers to see that!), in my mind, the 7th P-QRS also appears – visibly – a bit too early for this pattern of sinus arrhythmia (though it’s not nearly as obvious as the interval that follows it). Looking at all the preceding R-R intervals, one feels that they are very close to the same interval.

    While there should be no question in anyone’s mind that, due to its earliness, beat 8 is a capture beat (which should also dispel any thoughts of 3rd degree AV block), I think that quite possibly beat 7 is also a capture beat. Which (to me) also means that beat 8 is actually a PAC that managed to conduct on through to the ventricles. Now, it should also be evident to everyone that a rather abrupt change (increase) in the junctional rate (H’-H’ interval) has taken place AFTER these two beats and, more specifically, after beat 8. I think that beat 8, in passing through the AV node and the junction managed to discharge and reset the junctional pacemaker which is now firing at a more accelerated rate. This frequently happens with junctional ectopic pacemakers and supraventricular escape beats.

    The longest sinus P-P interval on this Lead II rhythm strip barely qualifies as a sinus bradycardia and most P-P intervals do not. The ectopic junctional pacemaker is also firing right at or above 60 beats/minute which is a bit beyond the upper limit for its escape rate. I wouldn’t think of this junctional rhythm so much as an “escape” rhythm (you can see that I’ve avoided using that term here) but more as an “accelerated” junctional rhythm. Most escape rhythms tend to be in the mid- to lower range of the ectopic escape rate – but that is based on my own experience.

    I would consider this AV dissociation to be due to usurpation rather than default because it persists even as the sinus rate increases. It might also qualify as AV dissociation by interference, though the episodes of AV dissociation may be a bit long for interference which is usually of very short duration.

    It’s wonderful to have a forum such as this to exchange ideas and to LEARN! I am very thankful to you and Drs. Smith and Meyers for this opportunity.

    Jerry W. Jones, MD FACEP FAAEM
    https://www.medicusofhouston.com

    ReplyDelete
  7. Hi Jerry. Thank you SO MUCH for your detailed commentary on this fascinating tracing. Unfortunately, this is the only ECG that we have on this patient — as I think some of the points you postulate might be much more easily resolved if we had a longer period of monitoring. While you and I do indeed agree on most points regarding this tracing — there are those points that we have different perspectives on. As you know, there is often more than a single plausible explanation for a given arrhythmia (especially when only a limited period of monitoring is available). So, there is not quite “gradual increase in the sinus rate” from beat #1-to-beat #7 (ie, the purple numbers in Figure 4 are my measured P-P intervals — and there is slight increase before decrease of these intervals). The junctional rate is right around 60/minute — Could that be the normal escape rate for this individual (I’ve always used 40-60/minute as the normal junctional rate — with 50-80/minute in a pediatric population — and this patient is a young adult … ). Moreover, distinction between AV dissociation by “default” vs “usurpation” is sometimes artificial, as it is not uncommon to have a mixture of both phenomenon. The reason I said “AV dissociation by default” in this case — is that the atrial rate IS slower than the junctional rate (purple numbers greater than blue numbers) at the time when junctional rhythm takes over. As to whether beat #8 is a PAC — We have “4 looks” at P wave morphology of beats #7 and 8 (in leads V1,2,3 and lead II) — and to me — P wave morphology in each of these 4 leads is quite similar — whereas if beat #8 was a PAC, I would have expected MORE variation in P wave morphology in at least 1 of these leads. And while your point about caution in using morphology of the QRS in a rhythm with AV dissociation to assess likelihood of conduction is an excellent one — I use this criteria VERY carefully (have done so for many years). I ONLY use differing morphology when it is truly consistent across the entire tracing — which is rare. Beat #2 is the only beat that does not fit the pattern here. Beats #3-thru-6 are all junctional beats — and NONE of them have either a small q or a shorter R comparable to R wave amplitude of other beats on this tracing. We BOTH agree that beat #7 is a capture beat (I indicated this above in my description). So while TRUE that we really do NOT know what the “true conducting PR interval is” in this case (ie, We just don’t have a long enough period of monitoring) — the inescapable findings I perceive are fairly marked sinus arrhythmia with sinus bradycardia — variability in the junctional escape rate — P waves conducting with different PR intervals — and a history of multiple episodes, some of which are presyncopal in a young adult with a positive family history of some unusual arrhythmia. To me, the most likely unifying theory would be excessive vagal tone, as in the syndrome of Vagotonic AV Block. So although there is NO evidence on this single tracing of frank AV block — the other features of this syndrome ARE present. I reference above a case on this syndrome that I wrote up (this is the link — http://ecg-interpretation.blogspot.com/2013/02/ecg-interpretation-review-61-av-block.html ). THANK YOU again for your wonderful comments. It’s always a pleasure to hear from you and debate interesting arrhythmia theories — :)

    ReplyDelete
  8. 1) Yes, AV junctional rhythm is very regular rhythm, but R5-R6 interval is slightly shorter than
    other junctional interval preceding it, and it is occurring during inspiration. That's why I
    said respiration is affecting even the junctional rate in this patient. But there is no question
    R6 is a junctional beat because the P wave is too close to the QRS. So, we pay attention to both
    the RR interval as well as the PR interval to decide whether the narrow QRSs are junctional or
    not. Ordinarily once you find out what the junctional interval is in that patient, any QRSs
    occuring with a short RR interval is not junctional.
    Beat 7,8 and 9 are definitely sinus beats because there is too much of jump in the RR interval.
    2) About thinking beat 8 as a PAC, it is true that the RR interval is noticeably short. But
    the P wave morphology of a PAC should be considerably different looking. This P wave is so
    identical to other P waves, and it is a sinus beat.
    3) Yes, in this patient the junctional rate is slightly faster than ordinary intrinsic junctional
    rate, which should be around 40-50/m. Therefore, strictly speaking, one should say slight
    junctional acceleration, rather than escape.
    4) All AV dissociation is by interference, i.e. two pacemakers interfering the progression of each
    other by rendering the myocardium or the conduction system physiologically refractory.
    K. Wang

    ReplyDelete
  9. Thanks for your reply, Ken. I always appreciate your thoughts. Although we DO have different perspectives on some aspects of this tracing, I think it is very telling that we each arrive at the same conclusion. And I agree with you TOTALLY about different ways to interpret a dysrhythmia. As evidence, just look at many of the laddergrams that Marriott or Fisch produced - sometimes 2 or 3 for the same dysrhythmia! I must say I chuckled a bit at your comment on dissociation by interference because I feel the same way. It's a lot like 2:1 AV block - it really isn't an entity unto itself but rather dissociation by default OR usurpation in a situation where one really can't decide.

    I'm glad to see your input on this blog and I look forward to many more productive discussions.

    Jerry

    ReplyDelete
  10. My sincere thanks to BOTH K. Wang and Jerry Jones — who are each specialists in arrhythmia interpretation of national and international renown. I’m always flattered and delighted to receive input from you both! I honestly believe the 3 of us agree on this tracing much more than the minor points in which our perspectives may differ. But what counts the most is this POSITIVE discussion in which specifics of this fascinating arrhythmia can be explored to the fullest. THANK YOU BOTH once again for your comments! — :)

    ReplyDelete
  11. Thank you for the amazing teaching on this post. Learned a lot.

    ReplyDelete

Recommended Resources