Wednesday, March 13, 2019

What is this rhythm? And what else does it show?

This was sent to me by my friend Sam Ghali (@EM_RESUS), https://twitter.com/EM_RESUS, with no information.

Sam frequently just sends ECG without saying anything else.  About anything! Which is always fun for me because when Sam sends one it is always a difficult ECG.

Here it is:
What do you think?

















These were my thoughts:

Rate and Rhythm: 
The rate is 126.  I see no definite P-waves.
There are two different morphologies of QRS.  Both are extremely wide, the 1st at 200 ms and the 2nd at about 160 ms.
The 9th beat (if you don't count the half beat at the start as the first one) is an early beat (a PVC), followed by the 2nd rhythm.  The PVC terminates one VT and starts another!
This is two different VT rhythms on the same 12-lead!

Ischemia?: V4-V6 have clear ST Elevation.

I wrote back:

I think this is VT with 2 different foci.
Beat 9 is an early beat that triggered the change, a PVC.
It also shows acute STEMI.

I sent this to Ken Grauer and he agreed.

Sam replied:

"Yup.  What's the culprit?"

I replied:

LAD

He replied:

67 yo guy. Altered, in shock. Looking at the chart apparently no actual CP but abdominal pain, SOB, etc. 

Yup. 100% Prox LAD (ostial).

March 14:

Now I see it differently, thanks to Christopher Watford's comment:

Alternative rhythm interpretation: ST w/ RBBB (small P-waves possible in leads I/III, approx 140 ms PRi), interrupted by a premature beat (focus unknown, possible fusion given intermediate shape), returning to ST w/ RBBB this time with LAFB due to the timing change by the premature beat.

I'm considering this as a possibility due to the identical rates of the first and second rhythms (both have RR's of approximately 470 ms).

I agree with LAD occlusion based on concordant changes in V4-V6.

Really neat ECG.



===================================
Comment by KEN GRAUER, MD (3/13/2019):
===================================
Fascinating tracing provided by Dr. Sam Ghali — enticingly without the benefit of any history. Having now looked at this tracing a 2nd time (and a 3rd time — and then a few more times …) — I have to amend my initial interpretation. I fully acknowledge that I do not know the etiology of this rhythm.
  • For clarity — I have labeled the beats in the long lead rhythm strip (Figure-1).
QUESTION: How would YOU approach interpretation of this arrhythmia?
  • HINT: Appreciation of ECG findings noted below will be greatly facilitated by use of calipers.
Figure-1: The very challenging tracing submitted by Dr. Sam Ghali. We are not given any history … (See text).
====================
MTHOUGHTS: Among the challenges posed in interpreting this tracing, is determining the width of QRS complexes. We know the QRS is wide. I wasn’t certain where QRS complexes ended — and where the ST segment in various parts of the tracing began ...
  • I have added vertical BLUE lines for each set of 3 leads in Figure-1 to show where I think the QRS complex ends.
There are 3 long lead rhythm strips in Figure-1— taken from leads V1, II and V5. It is probably easiest to appreciate events by focusing on the long Lead IRhythm Strip:
  • The rate of the rhythm is ~130/minute.
  • As per Dr. Smith — there are 2 different QRS morphologies. The first 8 beats in the long lead II manifest a small q wave with a predominantly upright, notched QRS complex ( = morphology Xas per the label above beat #8). Beats #10-thru-21 in the long lead II manifest a predominantly negatively notched QRS complex ( = morphology Zas per the label above beat #10).
  • The QRS complex for both of these 2 morphologies is wide. Assuming we are not dealing with hyperkalemia or some other toxicity — this suggests we are either dealing with a ventricular rhythm (or rhythms) — or, a supraventricular rhythm with one or more conduction defects.
  • I do not see clear sign of P waves. One can question whether there is a small, upright P wave preceding beat #10 — but if so, I did not appreciate this anywhere else. I therefore assumed no atrial activity.
  • Beat #9 occurs earlyWithout calipers — it is probably easiest to appreciate that beat #9 occurs early by looking from beat-to-beat in the long lead V5 rhythm strip. With calipers — you’ll instantly measure the shorter R-R interval preceding beat #9. It is right after this early beat — that beginning with beat #10, QRS morphology changes.
  • Morphology of both the QRS complex, as well as of the ST-T wave of beat #9 complex Y”) in the long lead II rhythm strip is intermediate between QRS and ST-T wave morphology of the beat that precedes it beat #8 = X”) — and the beat that follows it beat #10 = Y”). This initially suggested to me, that beat #9 with its intermediate morphology is a Fusion beat — which if true, would identify at least one of the tachycardias as ventricular in etiology.
MInitial Impression of the Rhythm:
  • As Dr. Smith noted above — my initial impression was that there were 2 wide tachycardias of different morphology — and that this represented 2 different foci of VT.
  • In support of this — there appears to be Selevation in leads V4V5 and V6 (seen to right of the vertical BLUE line in these leads, that marks the end of the QRS complex). A large acute STEMI, as this ST elevation seemed to suggest — would provide a reason to develop VT.
M2nd Impression:
  • I looked again at the QRS morphology we are provided with for beats #1-thru-5 in leads I, II, III; and V1 and V5 (seen to the left of the vertical LIGHT BLUE line in these leads). This QRS morphology is clearly consistent with a RBBB, in addition to the presence of multiple Q waves. The qR pattern in leads II and III, in association with the S wave in lead I is almost consistent with LPHB (usually the S in lead I is deeper with LPHB). Given the apparent absence of sinus P waves — perhaps this represented junctional tachycardia for beats #1-thru-8 (with bifascicular block as a consequence of the large ongoing STEMI) — with a Fusion beat ( = beat #9) — followed by a run of VT ( = beats #10-thru-21)?
M3rd (and FinalImpression:
  • I initially thought the rate of the 1st tachycardia (ie, beats #1-thru-8) was different and slightly slower than the rate of the 2nd tachycardia (ie, beats #10-thru-21). However, on careful measuring (and remeasuringwith calipers — other than beat #9, which occurs early — the R-R interval of all other beats on this tracing is identicalThe finding of identical rates for runs of beats with different QRS morphologies is rarely due to chance. I therefore think that despite the apparent fusion beat ( = beat #9) — that there is a single tachycardia occurring in Figure-1.
BOTTOM LINE: don’t know for certain what this rhythm is. Opinions from any electrophysiologists (or others who may be wiser than me) as to what may be going on are welcome!
  • Regardless of the rhythm — there appears to be lateral chest lead ST elevation consistent with a large ongoing STEMI. (This was borne out by cath results provided by Sam Ghali — which showed 100% proximal LAD occlusion).
  • Could the rhythm in Figure-1 be a single supraventricular tachycardia with underlying RBBB — that then manifests changing conduction defects (ie, switch to LAHB conduction following the early beat #9)?
  • Could there be atrial activity that we are just not seeing well due to lots of baseline artifact?
  • Could the rhythm in Figure-1 be some unusual form of VT (ie, Bundle Branch Reentrant VT — or some other form of reentry, perhaps through an occult accessory pathway)?
  • COMMENT — Sometimes, one has to proceed clinically despite uncertainty about the precise rhythm. Apparently, this patient was in shock on presentation. If so, given lack of sinus P waves — immediate cardioversion of this wide tachycardia would seem indicated regardless of the mechanism of the rhythm. Hopefully, this would result in conversion to sinus rhythm — at which point attention to the ongoing STEMI could be addressed.
  • Some of the best ECG learning cases are those in which we don’t have a definitive answer.
====================
FOR MORE:
  • For more Fusion Beats, and what they mean — CLICK HERE.


ADDENDUM: GREAT comment by Christopher (below) — which I am reproducing here. For clarity — I’ve added arrows for potential atrial activity (Figure-2).

Figure-2: Christopher’s comment + addition of arrows to my Figure-1(See text).
====================
  • I previously pointed out the possibility of a P wave following the early beat, occurring before beat #10 (BLUE arrow). The reason I was not convinced this was a sinus P wave — was that I didn’t (and still don’t) see any indication of sinus P waves preceding beats #1-thru-8 in this long lead II, despite the isoelectric baseline with more than enough space to fit a P wave in before these first 8 beats ...
  • That said — as per the PURPLE arrows ( = Christopher’s theory, which is perhaps the most plausible) — there is suggestion of a small deflection preceding beats #11-thru-21.
  • As per my “3rd Impression” — the identical rate for both QRS morphologies that we see in this tracing is unlikely to be due to chance — and strongly argues that there is one single tachycardia here, which most probably results from acute STEMI with sinus tachycardia RBBB (for beats #1-thru-8) — followed by the early beat (not a “fusion” beat, despite looking so much like it is fusion ... ) — which due to the shorter recovery time precipitates LAHB in addition to RBBB for the last 12 beats in the tracing. THANK YOU Christopher!



24 comments:

  1. How did you know it was LAD ?

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  2. Alternative rhythm interpretation: ST w/ RBBB (small P-waves possible in leads I/III, approx 140 ms PRi), interrupted by a premature beat (focus unknown, possible fusion given intermediate shape), returning to ST w/ RBBB this time with LAFB due to the timing change by the premature beat.

    I'm considering this as a possibility due to the identical rates of the first and second rhythms (both have RR's of approximately 470 ms).

    I agree with LAD occlusion based on concordant changes in V4-V6.

    Really neat ECG.

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    Replies
    1. Christopher, I think you're right. I now see a P-wave preceding the beat directly after the PVC.
      Thanks!
      Steve

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    2. What mistake am I making in seeing evidence of p-waves in V1?

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    3. GREAT comment Christopher. I have added it with an illustrative figure as an ADDENDUM (above) to my comment — THANK YOU — :)

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    4. You ARE seeing P-waves. My mistake.

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    5. Can LAFB change V1 and V5 morphology so much?

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  3. Question, in v6 there seem to be notches prior to the QRS complexes, why are those not p waves?

    Also, Why would hyperkalemia not be a consideration as the QRS complexes seem to be wider than usual, is it because the lateral leads have elevations?

    Thank you very much for this post and the others, I learned a whole lot from you.

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  4. Very interesting ECG! QRS widening often makes the recognition of STE problematic because it's often mistakenly written off as part of the QRS.

    Steve, I don't think this represents two separate VTs for two reasons: 1) The rate is exactly the same before and after the PVC which would be unusual (though not impossible) for two separate ventricular ectopic sites and 2) a single ventricular focus that changes its exit site after a PVC would be much more feasible (and frequent) than two distinct VT sites firing at exactly the same rate. I think the PVC caught the usual exit site before the myocardium around it had a chance to repolarize thus lengthening the effective refractory period long enough to allow the myocardium around a second exit site enough time to recover and conduct. And I certainly don't think this represents bundle branch reentry because the QRS intervals are usually more narrow, the rate a lot faster and the PVC probably would have interrupted the reentry circuit.

    It's very interesting that - if you look at the rhythm strip of V1 - you see no good evidence of STE until AFTER the PVC when it suddenly becomes much more obvious. That is probably because the direction of the ventricular depolarization from the first exit site caused it to be confounded with the QRS.

    I always instruct my ECG students to never assume that a VT "just happens!" Always look for a cause - like an acute STEMI! Great case. My thanks to Dr. Ghali for letting us learn from it.

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  5. Steve...

    I just printed out the ECG and took a closer look. Take another look at the Lead II rhythm strip. The pause that follows the PVC is COMPENSATORY and there appears to be a well-formed P wave following the T wave of the PVC. You can see a similar simulataneous P wave in aVF. I'm wondering if the PVC didn't just cause a change in the preferential conduction down the contralateral bundle branch.

    Jerry

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  6. My eyes went nuts trying to find a p wave.

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  7. always enjoy and learn from your posts, even though i am now retired. It keeps my brain active and keeps me from losing all I used to know.

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  8. Where do you measure the ST elevation in V4-V6? No matter how much I look at them, they look like wide QRS complexes without any T waves to me?

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    Replies
    1. Ken Grauer has drawn vertical lines at the end of the QRS, which is the beginning of the ST segment

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  9. Where do you measure the ST Elevation in leases V4-V6? No matter how I look at them all I can see is a very wide QRS complex with none or minimal T waves.

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  10. Wow what a great discussion guys.

    I do think Christopher’s interpretation is likely the most accurate. The rates of the rhythm before and after the premature beat are definitely the same and point overwhelming to a single tachycardia focus. The rhythm makes the most sense to be supraventricular in origin and I do think probably sinus. The other clue that speaks against VT is the morphology for RBBB is classic. Further the appearance for RBBB + LAFB is also classic in terms of morphology, QRS lengthening, & the accompanying axis change is consistent as well. The only thing I would say different is that Christopher suggested the premature beat that seems to trigger the LAFB may be a “fusion” beat which doesn’t really make sense here in the absence of VT. But I do think its morphology is too similar to the other beats and does appear to be such an “intermediate form” of the other two, that I think it would be too bizarre of a coincidence for this to randomly be a PVC with similar so morphology. My best guess is that it’s a premature supraventricular beat (perhaps junctional) that conducts with an incomplete LAFB on that one particular beat and thus producing the intermediate form QRS.

    Thanks so much for all your thoughts. It's amazing what can be figured out when minds come together.

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  11. GREAT discussion by all. I think at this point we ALL agree this is 1 (not 2) tachycardias — and that the tachycardia is supraventricular — initially with RBBB — and later with RBBB/LAHB morphology. Two points to emphasize: i) While morphology is clearly consistent with RBBB (given the wide upright complex in V1 and the wide terminal S wave in lead I) — it’s important to realize that it is NOT “typical” for RBBB — because there is NO terminal S wave in lead V6. I’ve seen this often with acute MIs — that you’ll then develop superimposed RBBB without a terminal S wave in lead V6 — but my point is that morphology in the chest leads by itself would be potentially consistent with either a supraventricular or ventricular etiology (OTHER factors, as noted — tell us that in this case it is supraventricular). ii) I still ask WHY if the PURPLE arrows in my Figure-2 represent sinus P waves — then WHY do we NOT see sign of sinus P waves in lead II for beats #1-thru-8? There is a lot of artifact in lead I — but it does look like there may be atrial activity in that lead — but with sinus rhythm, you SHOULD see upright P waves in lead II — and given the identical heart rate for 1st and 2nd parts of this tracing — it doesn’t make sense to postulate shift from a different atrial focus. So WHY sinus P waves after beat #10 but not before? My point in raising these 2 issues is that EVEN THOUGH we all seem agreed on the most logical conclusion for this tracing — there ARE still factors that I believe are not totally explained on this single tracing. I bet that availability of 1 or 2 additional tracings from this patient would definitively answer all issues. Again — GREAT discussion by ALL! — :)

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  12. Ken great comments, absolutely agree. I should clarify by saying this RBBB is indeed very abnormal! In fact we’ve talked so much about the rhythm that we should emphasize: this is a RBBB with STEMI in a patient who had 100 % Proximal LAD Occlusion!

    Bc I have seen several cases of RBBB + LAFB + LAD Occlusion, (as I’m sure you have as well) I recognize this morphology as classic but only for this in this scenario with this combination. In fact I recently tweeted a case with RBBB + LAFB + LAD Occlusion. Yes the S waves in V6 are obliterated by the ST Elevation! By the way you can see the ST Elevation very nicely in the right precordial leads on the ECG, with the very Shark Fin-like elevation in V2.

    With regards to the rhythm: On beats #1-8, I think the P waves are there in Lead II. The question is: are they upright in Lead II? You can see them fairly clearly in Lead I with a constant PR interval. You can also see them fairly well in Lead III and they are inverted in this lead. The PR intervals and P-P intervals are constant throughout this ECG. If you draw vertical lines down in Lead II to the V1 rhythm strip (as opposed to V5 as you have done) I think you will see that the P waves in V1 are upright and your blue arrow points not to an upright P wave, but rather to an upright deflection AFTER an inverted P wave - and your purple arrows follow suit. So given this P wave axis, I think the rhythm is actually likely to be Atrial Tach!

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  13. Really GREAT discussion on a tough tracing.
    I think we have more questions than answers and additional and more prolonged monitoring would be useful; anyway let me add my take hopefully interesting despite many great interpretations have already been made.
    What seems to be sure is 1) STEMI and 2) artifacts; the latter finding could justify some of our difficulties in interpreting the rhythm (I refer to atrial activity of course).
    That said, I strongly favor the diagnosis of sinus tachycardia with aberrant conduction (or pre-existing bundle branch block).
    My interpretation (=speculation) is based on the following conjectures: the RBBB morphology favors the diagnosis of a SVT rhythm since it looks typical: rSR' in V1 (in all beats), terminal and delayed S wave in lead I. But why is the S wave lacking in V5-V6? I think that the ST elevation in those leads deforms the terminal part of the QRS thus cancelling the delayed S wave; interestingly the premature beat #9 shows a terminal S wave in aVL. Hence I still think the RBBB pattern is typical and as a consequence the rhythm is more likely supraventricular.
    Atrial acitivity: as mentioned above some of our troubles are due the presence of artifacts, especially in the most important lead II; moreover we all agree that there is a clear sinus P wave preceding beat #10. That said and despite the presence of artifacts, I suspect that signs of atrial activity are present in several leads and the use of calipers make easier measurements. As per Ken Grauer's figure, I see too signs of atrial activity from beat #11 to #21 (constant PR interval): if we apply the same PR interval to lead I,I think we can affirm that in this lead too the underlying rhythm might be sinus tachycardia.
    Finally how to concile the premature and mysterious beat #9? Is it a PVC? Or a PAC with simultanoeus activation of the ventricles by the supraventricular impulse with a PVC? Really I don't konw.
    Rosembloom once said that “Every self-respecting rhythm has at least 3 possibile explanations!”

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  14. THANKS so much Sam for following on the questions I posed. I will respectfully disagree with you — because after spending literally HOURS studying this case (and rewriting more than twice my comments …) — I just do NOT see consistent deflections (ie, fully reproducible and unequivocally distinguishable from baseline artifact) in the way you describe. I also contemplated the possibility of atrial tachycardia — but felt (and still feel) that the probable atrial activity represented by the BLUE and PURPLE arrows in my Figure-2 looked different from what I saw in BOTH simultaneously recorded leads V1 and lead II — and given the identical rate at the beginning and end of this rhythm strip — I didn’t see how the atrial focus could shift. So, YES — I do see what looks to possibly be a negative deflection in lead III for the first 4 complexes in that lead — but not in the 5th, and not in any of those first 3 complexes in lead aVF (which typically shows similar atrial deflections as in lead III). I still think ( = my opinion) my upright BLUE arrow in front of beat #10 represent a sinus beat — but I still don’t understand why when the baseline for the 0.16 second in front of the QRS for beats #1-thru-8 is flat, why we don’t see an upright sinus P wave preceding beats #1-thru-8 … BOTTOM LINES: #1) I think [ = my opinion] as per Mario [who commented just after you] — that the artifact makes it impossible for any of us to be certain of what we are seeing for each beat on this tracing; #2) Also per Mario = “There is more than a single possibility here”; #3) The clinical scenario of proximal LAD occlusion commonly manifests with RBBB/LAHB as we see here; and #4) As is OFTEN the case in my experience — it is VERY likely that a definitive answer to all that appears on THIS fascinating tracing WOULD BE forthcoming IF we had in front of us just a few more ECGs recorded just before or after this tracing. That said — THANK YOU so much Sam for this fascinating contribution — and THANKS to ALL commenters for a superb discussion! — :)

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  15. Thank you Ken! I think we agree much more than we disagree! There's little regarding the rhythm that I am absolutely certain about. I just blew the ECG up again and took another look drawing vertical lines and measuring. My interpretation is based on what evidence we have but yes there is too much artifact and we are definitely dealing with a high degree of speculation and deductive reasoning and I totally agree I do not think it's possible for us to know the definitive rhythm based on this tracing. Great demonstration of the limitations of surface ECG! I know for sure there was no prior ECG but I will look and see if I can get a follow up one and if so I will send it on to Steve. Thanks again!
    Best,
    Sam

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    Replies
    1. Hi Sam. I AGREE — there is MUCH MORE that we agree on — and the rest relates to stuff that I don't think anyone can know for certain. Great discussing with you! — :)

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