The initial ECG from the urgent care shows a very fast rate and what appears to be a wide QRS. Further inspection of leads V1 and V3 show what seems like a discernible p wave in conjunction with the QRS. This would rule out that the rhythm was ventricular in nature. I did some research and determined that the reason why the QRS is wide is due to the conduction being AV re-entrant and the ventricles are being activated through the accessory pathway.  It is also antidromic due to retrograde conduction going back to the atria through the AV junction.

The followup ECG after the pt converted shows a typical WPW pattern with delta waves visible in lead V2.  Very fascinating. 

One thing I immediately noticed about the ECG of the wide QRS complex tachycardia is that something doesn't look quite right about the transition in the precordial leads.  Lead V1 shows a diphasic rS complex that is predominantly negative.  V2 is a large monophasic R-wave that is wholly positive.  V3 is now back again to a diphasic rS complex.  (S.G.) even makes a point of jumping over lead V2 in order to draw attention to what they think is a P-wave in only those two particular leads.  It stands to reason that if a P-wave is going be visible in both V1 and V3, then is should be equally visible in V2 as well (maybe even more so).  Lead V4-6 are all back to being predominantly positive again.  This "staggered" look and lack of normal QRS transition seems out-of-place and not at all natural to my eye.  I think that in the heat of the moment, someone attached a precordial cable (or two) to the wrong electrode.  I'm not convinced there are any visible P-waves or other atrial activity here.  As it is, I don't think there's any way to completely rule out the possibility of this being monomorphic ventricular tachycardia. 

I do however agree with the interpretation of W-P-W on the ECG displaying sinus rhythm and I think the wide QRS complex tachycardia is probably some form of preexcited tachycardia (probably antidromic tachycardia over a right-sided accessory pathway assuming, of course, that V1 is correctly attached to the right electrode).    

It's kind of scary how the computer says there is a signal problem when the ECG is of high quality and free of artifact.  Furthermore, why would the computer consider this to be sinus tachycardia at a rate of 222/min???  

 My first thought on looking at the WCT tracing was that it looked like WPW with flutter EXCEPT that the rate (~ 220/minute) is clearly slower than the ~300/minute expected with flutter. Therefore - IF this was the ONLY tracing you had - VT should clearly be assumed until proven otherwise. That said - (S.G.) gave us the history that the patient has known WPW - and this is confirmed in the post-conversion tracing. In view of this - I feel this tracing is much less likely to represent VT.

• My ECG Blog #18 reviews the potentially problematic arrhythmias commonly associated with WPW. Given that the patient in this case has known WPW-associated arrhythmias - it is highly likely that the regular WCT at 220/min seen here is PSVT with antidromic conduction. As discussed on my ECG Blog #18 - PSVT virtually always conducts orthodromic (~95% of the time!). On those rare instances when it conducts antidromic - it may look identical to VT !!! In such cases, it may only be AFTER conversion that one is able to distinguish between VT vs WPW with antidromic conduction and a wide QRS ...

• Cardioversion was the correct clinical move. Lidocaine would not have been advised - but the patient did ok despite that.

• Lead V2 is OFF. I can't imagine any scenario in which V2 makes sense. My thought is identical to Jay's - namely, that in the heat of the moment someone just picked up the wrong lead (since V2 would make sense if it was a lateral precordial lead ... ).

• There are NO P WAVES on the WCT tracing. Even though V2 is misplaced - it's TIMING is correct - and it is easy to drop a vertical timeline confirming that what was thought to be a "P" is really the T (so this was one GOOD thing that came out of misplacing lead V2 - in that it makes it EASY to confirm that there are NO P waves !!!! ).

• The post-conversion tracing is fascinating. The last part of the QRS in a WPW tracing is really a "fusion beat" - after the delta, when the impulse hooks up with the remaining portion of the conduction system - and I can almost see this in the post tracing where V1's terminal part looks similar to V1 during WCT. V3 is off - but note the early transition and then reduced QRS amplitude in lateral precordial leads which to me corresponds to the reduced QRS amplitude in the lateral precordial leads during the WCT. And, leads I and III during WCT look similar to the post-conversion tracing leads I and III. Lead II is different - but not unlike the difference that often is seen with a slight axis shift.

• The post-conversion tracing to me shows worrisome ST-T wave changes in several leads (especially in V2). Of course, one can NOT draw any firm conclusions re ST-T morphology in the post-conversion tracing given that there is AP (accessory pathway) conduction - but ST-T waves like the QRS show "fusion" in the post-conversion tracing - and the ST changes in this post-conversion tracing to me are clearly more than I'd expect for simple WPW .... That said - there is a well known "post-tachycardia T wave syndrome" - in which the tachycardia itself may alter ST-T morphology in a post-conversion tracing - so there is NO WAY to know for sure what is truly going on. Troponins are clearly indicated from what I see. Realizing that slight troponin bumps are common following prolonged tachycardia - I'd be looking for a BIG increase in troponins before concluding that an ischemic (or worse) event occurred.

• Re computerized readings - the computer is far from perfect