Fascinating case because of the difficulty in figuring out what is going on. This is what happens with “real life tracings” — in which acutely ill patients may not allow obtaining the artifact-free ECG that we seek.

My assessment mirrored Dawn’s throughout the case. I thought the initial ECG represented a regular WCT ( = Wide-Complex Tachycardia) at ~170-180/minute, without clear sign of P waves. Inability to define the limits of the QRS complex made me question a ventricular vs supraventricular etiology, without clear answer. The frontal plane axis was indeterminate (predominantly negative in leads I and in all inferior leads) — but the presence of a tiny-but-real initial r wave in all leads greatly reduced the diagnostic utility of this frontal plane axis deviation. It is only when the QRS complex in either lead I or lead aVL is entirely negative — that frontal plane axis becomes strongly predictive of VT.

QRS morphology in lead V1 is upright, which is consistent with RBBB (as are the terminal wide S waves in lateral leads) — but the QRS complex in lead V1 looks more like a “blob” than an RBBB pattern. And, the initial r wave deflections in leads V3-thru-V6 were narrow — which weighed against VT. Finally — I was undecided about how much of the seemingly widened S waves in leads V3-thru-V6 might actually reflect ST segment depression.

BOTTOM LINE: Given that this elderly patient had signs of hemodynamic instability — I agreed with the initial management approach of IV amiodarone and synchronized cardioversion.

I once again shared Dawn’s concerns on seeing the post-cardioversion ECG. As per Dawn — QRS morphology was virtually unchanged despite clinical improvement, reduction in heart rate — and what also looked to me despite the artifact, as probable sinus P waves in the inferior leads. This led me to the same conclusion as Dawn — that this patient was not adequately perfusing with his initial wide-complex rhythm because of AVNRT at ~170-180/minute — and that the result of amiodarone followed by synchronized cardioversion appears to have been restoration of sinus rhythm.

FINAL THOUGHT on the ECGs: I almost wonder if Brugada phenocopy was superimposed on underlying RBBB — as this might account for the bizarre QRS morphology we saw in lead V1. Alas, answers to my curiosity require the follow-up tracings that unfortunately are not available to us.

MORAL of Today’s Case: Definitive answers are not always possible with “real” cases. Sometimes clinical management decisions have to be made without being certain of the etiology of the initial rhythm, as was true in this case. IV Amiodarone and synchronized cardioversion were indeed appropriate measures in today’s case, even though we were in no way certain of the initial rhythm.

I spent an hour tonight reading an old issue of "Heart Rhythm Journal (July 2010, Vol 7, Issue 7) plus some follow through on lifeingthefastlane.com, where the topic was R-Wave Peak Time in Lead II, to help differentiate VT & SVT. On ECG #1, the RWPT on Lead II is clearly less than .50 ms (which favors SVT). The patient was clearly unstable and acutely symptomatic thus guiding the EMT's to opt for amio and cardioversion; luckily achieving a slower heart rate looking like S. Tachycardia. My guess is that it was an Atrial Tachycardia but the quality of ECG's obtained in the field do often have a lot of artifact. 

Great presentation!

Thiis today's case demonstreates that most criteria for VT are not perfect (low specificity) when the patient's baseline ECG (I assume that the ECG during sinus rhythm was patient's baseline tracing) shows conduction abnormalities.

Thanks for presenting!

Very interesting case, Dawn. I like seeing ECG tracings that are less than pristine because that is what you get in real life. I include them in my classes. My initial feeling was that this represented an SVT. There were a number of small r waves (as Ken pointed out) in left-sided leads which indicated an impulse traveling from right-to-left and less convincing of ectopy (in my experience ectopic depolarizations aren't likely to change directions 180 degrees!). The downslopes of the S waves were quite straight and relatively smooth. The cardioversion to the same QRS morphology indicated an AVNRT to me as well. Cardioversion would be very unlikely to work on an atrial tachycardia unless it were a very rare reentrant type (most are automatic and immune to cardioversion).

I agree with Mario in that all algorithms and methods have their shortcomings. Personally, I hesitate to use any single-step method because that is putting all the patient's eggs in one basket. And the Lead II R Wave Peak Time is slightly prone to diagnose v. tach as SVT - a very dangerous situation.

Keep up the good work and I enjoyed finally meeting you "in voice" during the webinar! (I'm still working on my ZOOM skills.)