This Case was sent by Atif Farooqi and Scott Weingart, from Stony Brook.
This is a 70-something with history of CABG who presented with 30 minutes of SOB and palpitations.
Here is his ECG:
Atif wrote this:
"My first thought was perhaps a bidirectional V Tach, though the pt is not on digoxin and otherwise has no discernable reason to be in BVT. Scott was considering maybe an intermittent aberrant conduction, though we thought it odd for it to be strictly alternating beats.
Here is my answer:
Atif,
Interesting EKG!
I think it is SVT with every-other-beat-aberrancy.
--Every QRS comes right on time, perfectly regular, so it can't be Bigeminy.
--Every
other beat is RBBB, which is the most common type of aberrancy because
the right bundle has a longer refractory period than the left.
--The inbetween beats are of normal duration (100 ms). The axis does not alternate. There is no alternating RBBB and LBBB. So it can't be bidirectional tachycardia (neither bidirectional VT nor bidirectional SVT).
--There are no P-waves.
So this is AVNRT with alternating aberrancy (Scott was right!).
Additionally, both the aberrant and the normally conducted beats have significant ST depression.
Bidirectional Tachycardia implies alternating frontal plane axis, from -60 to +120, or alternating LBBB and RBBB.
Bidirectional tachycardia can be Bidirectional Ventricular Tachycardia, as with Digoxin toxicity. The etiology may be:
1. alternating location of origin of the VT ectopic focus, or
2. alternating routes of depolarization from a single ectopic focus
Bidirectional VT may also result from aconite toxicity, as in this case I reported, which has alternating RBBB and LBBB.
Bidirectional Tachycardia can alternatively be due to SVT with Bidirectional Aberrancy: the aberrancy may be due to:
1. RBBB with alternating LAFB (left axis) and LPFB (right axis), or
2. Alternating RBBB and LBBB.
Here is the ECG from this case of Aconite Toxicity:
This case presented here today does NOT have alternating frontal plane axis, nor does it have alternating RBBB and LBBB, so is not bidirectional tachycardia.
Case continued:
The attending gave IV Metoprolol, (the patient was supposed to be taking oral metoprolol as an outpatient), and the rhythm changed to the following:
This is a 70-something with history of CABG who presented with 30 minutes of SOB and palpitations.
Here is his ECG:
What is it? |
Atif wrote this:
"My first thought was perhaps a bidirectional V Tach, though the pt is not on digoxin and otherwise has no discernable reason to be in BVT. Scott was considering maybe an intermittent aberrant conduction, though we thought it odd for it to be strictly alternating beats.
Here is my answer:
Atif,
--Every QRS comes right on time, perfectly regular, so it can't be Bigeminy.
--There are no P-waves.
Additionally, both the aberrant and the normally conducted beats have significant ST depression.
Bidirectional Tachycardia implies alternating frontal plane axis, from -60 to +120, or alternating LBBB and RBBB.
Bidirectional tachycardia can be Bidirectional Ventricular Tachycardia, as with Digoxin toxicity. The etiology may be:
1. alternating location of origin of the VT ectopic focus, or
2. alternating routes of depolarization from a single ectopic focus
Bidirectional VT may also result from aconite toxicity, as in this case I reported, which has alternating RBBB and LBBB.
Bidirectional Tachycardia can alternatively be due to SVT with Bidirectional Aberrancy: the aberrancy may be due to:
1. RBBB with alternating LAFB (left axis) and LPFB (right axis), or
2. Alternating RBBB and LBBB.
Here is the ECG from this case of Aconite Toxicity:
Alternating RBBB and LBBB. Intervals are regular. |
This case presented here today does NOT have alternating frontal plane axis, nor does it have alternating RBBB and LBBB, so is not bidirectional tachycardia.
Case continued:
The attending gave IV Metoprolol, (the patient was supposed to be taking oral metoprolol as an outpatient), and the rhythm changed to the following:
Wonderful case for discussion, that I believe can be confidently identified as AVNRT from the initial tracing. The rhythm is a regular tachycardia at ~ 170/minute without sign of sinus P waves. There is QRS widening on alternate beats. The reason we can be confident this is AVNRT from review of the first tracing alone — is that the initial QRS deflection in all leads is the same (both in direction as well as in slope).
ReplyDeleteThe wide beats strongly suggest a supraventricular rhythm with RBBB conduction because: i) there is a typical rsR’ complex in lead V1 with s wave that descends below the baseline and taller right (R’) rabbit ear; ii) there are wide terminal S waves in leads I and V6 — with an initial R wave in these lateral leads that is slender and normal in appearance; and iii) there is a qRS pattern in lead I, which serves like a “reciprocal” to the rsR’ in lead V1 that is characteristic of RBBB conduction. We can debate as to whether there is also LAHB (left anterior hemiblock) for all beats on this tracing (probably), and perhaps incomplete RBBB for the narrower beats — but regardless, QRS morphology for the wider beats is strongly suggestive of complete RBBB.
With normal ventricular depolarization — the left side of the septum depolarizes first. Since the slender right bundle branch courses down the right side of the septum — septal depolarization, and left ventricular depolarization that follows normal septal depolarization are unaffected when the right bundle branch is non-functional. This explains why RBBB is a “terminal delay”. It is only after the septum and LV (left ventricle) have depolarized, that the electrical impulse is finally able to make its away over to depolarize the RV (right ventricle). This also explains why the comparatively small RV often produces a surprisingly large R’ deflection in lead V1 — because RV depolarization is unopposed with RBBB since LV depolarization has already been completed. Awareness of this sequencing is helpful for recognizing RBBB aberration — since the initial part of the QRS complex is typically unaffected when there is RBBB. This is precisely what we see here. Note in lead V1 that the small initial r wave AND the beginning of the descent to the s in this lead is identical both for the narrow and wide beats. The same is true in virtually all other leads — as only the terminal portion of the QRS complex is altered. This appearance is virtually diagnostic of alternate RBBB conduction. When RBBB aberration occurs, it most often is seen with each beat in the tachycardia. However, on occasion — RBBB aberration may only be seen every second- or every third beat in the tracing — and that is the situation here.
Our THANKS to Atif Farooq and Scott Weingart for sending this interesting tracing to Dr. Smith for publication in Steve excellent ECG Blog.
Very interesting ECG.
ReplyDeleteWhat about vagal maneuvers as first diagnostic/therapeutic approach?
Many thanks
Sure, that might work. The modified Valsalva with leg raise has 40% efficacy.
DeleteI've tried the modified Valsalva three times without success... I may have to read the REVERT trial once more to make sure I'm doing it right..
DeleteNice ECG! It does seem to be BVT at the first glance
ReplyDeleteIf 1st ECG is regulr, aberrancy is impossible.
ReplyDeleteI think ventricular electrical alterans is right.
What do you think about electrical alterans?
No. It is alternating normal conduction with aberrant conduction. The post conversion ECG proves it.
DeleteDear Anonymous — Please also be sure to read my detailed comment (above yours). We both absolutely prove that there was aberrant conduction — :)
ReplyDeleteWhat do you think about the STE in aVR and V1? ST depression are reciprocal? Tx
ReplyDelete