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:


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).
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 Fusion Beats, and what they mean — CLICK HERE.

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