Wide Complex Tachycardia -- VT, SVT, or A Fib with RVR? If SVT, is it AVNRT or AVRT?

A 69 y.o. male with pertinent past medical history including Atrial fibrillation, atrial flutter, cardiomyopathy, Pulmonary Embolism, and hypertension presented to the Emergency Department via ambulance for respiratory distress and tachycardia. 

Per EMS report, patient believes he has been in atrial fibrillation for 5 days, since coming down with flu-like illness with rhinorrhea, productive cough, SOB. Patient is on rivaroxaben, carvedilol, and dofetilide (to suppress atrial fib -- rhythm control).  He states that he maybe missed a dose or two during recent illness. On EMS arrival, patient's oxygen saturation was in the high 80s and improved on 4L O2 via nasal cannula. 

He was noted to have irregular heart rhythm with rates 120-170s. BG 248. 

Bedside ultrasound showed volume depletion and no pulmonary edema.

Here is the prehospital ECG:

First ED ECG

What do you think?

Description: Regular Wide Complex Tachycardia at a rate of about 160.  VT?  SVT with aberrancy?  If SVT, is it AVRT or AVNRT?  It appears too regular to be atrial fib with RVR

I inspected this carefully and it is very regular.  Thus, it really cannot be atrial fibrillation

Is it Ventricular Tachycardia, which is usually a regular rhythm?

Smith opinion: I at first thought this was VT and would have electrically cardioverted.  But I changed my mind after seeing the old ECG (below)

I later sent it to Ken Grauer, who annotated as below with the red Xs:

The "Y" in lead II across the bottom appears to be a PVC.  

Thus is it almost impossible that this is VT, even without the old ECG.  Since it is regular, it must be PSVT (AVNRT or AVRT).    

Thus, adenosine is very likely to work here.

 

______________________

If you want to know more detail (skip if you do not need so much detail), especially if it is AVNRT or AVRT, Ken writes the below, where he also agrees that it cannot be atrial fibrillation:

There are 2 places with this otherwise very regular WCT is “interrupted”. The 1st place ( = X) is kind of bizarre, in that QRS morphology look very similar in leads I,II,III — but a little earlier and narrower (almost like this beat may have occurred during the “supernormal conduction” period ( = a truly RARE phenomenon).

But the 2nd interruption = Y — looks to be a PVC — which is why, even before seeing the prior tracing, I suspected this initial ECG was supraventricular (and not VT).  

Smith: this is because it is almost impossible to have a PVC in the midst of VT

I measured intervals with calipers on my big screen — and other than these 2 interruptions, find the rhythm VERY regular. I don’t see evidence of retrograde atrial activity during the WCT — but usually with the “almost regular AFib rhythms” — you can when you measure pick up some slight differences — so my hunch is that the initial ECG is a REENTRY SVT rhythm, that then breaks down to AFib.

Now you CAN on occasion see PVCs during reentry SVTs that do not convert the SVT. Theoretically  — this can occur with BOTH AVNRT and AVRT. In theory, a PVC is more likely to convert AVRT — because part of the reentry pathway is OUTSIDE of the AV Node (ie, passing thru the AP) — and therefore a PVC would be more likely to “run into” the reentry pathway, and convert the rhythm.

In theory, with AVNRT — the reentry pathway is completely contained WITHIN the AV node — so a PVC would seem LESS likely to convert AVNRT, because it “can’t get to” the reentry pathway that is entirely within the AV node — so my hunch is this initial ECG was AVNRT ________________________

The patient was stable enough to look for a previous ECG.  Here it is:

Slow atrial fibrillation, rate controlled with carvedilol presumably

This shows the same QRS morphology (RBBB + LPFB), proving that the rhythm above is supraventricular, and NOT VT (as suspected by the PVC)

The providers realized it was not VT, but did not recognized it as SVT with RBBB/LPFB.  Instead they diagnosed it as Atrial Fib with RVR.

Thus, they did not give adenosine.

A patient who has atrial fib and is on dofetilde is on a "rhythm control" strategy for AF.  Dofetilide is used for atrial fib rhythm control, not for rate control.

The appropriate management would be to give IV fluids first to restore volume in this patient whom they believed had pneumonia as the initiating factor.  I'm not sure if they started with this, but let's assume that they did.

If you think this is atrial fibrillation with RVR, then because the patient is anticoagularted, one could safely sedate and cardiovert.  Of course, this is NOT atrial fib, but rather PSVT, and so adenosine should work. (Some are now advocating for calcium channel blockers, but that discussion is for another day).

The patient did not want to be electrically cardioverted, so they gave metoprolol.

t = 14 minutes, after giving IV metoprolol

Now there is atrial fibrillation with a much slower rate and PVCs.

Metoprolol can sometimes convert SVT, and sometimes the rhythm can change to atrial fibrillation.

t = 16 minutes

Further Care in the ED:

1. Patient hemodynamically stable, discussed options with patient, would prefer medications before attempting cardioversion
2. Patient given metoprolol 5 mg IV with improvement in HR to 110-120s, repeated ~q5 mins x3. Patient also given metoprolol PO 50 mg. 
3. Mag 2g administered 
4. Appeared mildly hypovolemic on US, LV function grossly preserved, reports decreased PO intake, given gentle 500 cc bolus
5. CXR with likely infiltrates vs edema, blood cultures collected, started ceftriaxone and azithromycin
6. Given patient reports not having taken home meds today, given home dofetilide, coreg and xarelto
7. Labs notable for mild Acute Kidney Injury (Cr 1.5). pH 7.4. 
8. CT noncon prelim consistent with pneumonia, final read pending
9. Patient's HR 110s, respiratory effort improved, reported symptomatic improvement

Later in afternoon

After a brief hospital stay, the patient was discharge, still in atrial fibrillation.

On a visit 2 months later, he was cardioverted.