ECG of the Week: ECG of the Week - 20th January 2014

This ECG is from a 76yr old who presented complaining of palpitations and dysponea.
Past medical history of paroxysmal atrial fibrillation and chronic smoking related lung disease.
Medications include warfarin, calcium channel blocker, and other non-cardiac related medications.
The first ECG below was performed when the patient arrived, the second ECG was performed not long after but prior to treatment being instigated.
Check out the comments on our original post here.

ECG 1 - Initial ECG on arrival to the Emergency Department

ECG 1
(Click to enlarge)

Rate:

~220 bpm

R-R Interval ~280ms

Rhythm:

Regular
Nil p wave visible

Axis:

Extreme Axis deviation

Intervals:

QRS - Prolonged at 120ms

Additional:

Precordial transistion lead V6
Extensive artifact obscures lead I

Impression

ECG features suggest origin in apical right ventricular septum

ECG 2 - Performed shortly after ECG 1 and prior to treatment.

ECG 2
(Click to enlarge)

Rate:

~220 bpm

R-R Interval ~280ms

Rhythm:

Regular
Nil P waves visible

Axis:

LAD (-45 deg)

Intervals:

QRS - Normal (80ms)
QT - 280ms

Segments:

ST Elevation aVR (2.5mm)
ST Depression leads I, II, III, aVF, V4-6

Additional:

Notching of terminal QRS / early ST segment best seen in leads II, III, V6

Interpretation:

AVNRT

Differential Dx of Atrial flutter with 1:1 conduction

ST segment changes

? Related to dysrythmia rate
? Ischaemic pattern of potential left main or severe multi-vessel disease

Challenging features

The spontaneous nature of the rhythm change in this case is both interesting and challenging to explain based on the ECG's.
The morphology of the broad complex tachycardia in the first ECG with the near identical cycle length in both dysrhythmia means a unifying pathological process is difficult to describe.
Whilst a 'slower' VT can precipitate a 'faster' SVT the identical cycle length of both rhythms does not support this mechanism.
The morphology of ECG 1 does not fully support a Mahaim pathway (antegrade conducting accessory pathways connecting either AV node to ventricles, fascicles to ventricles, or atria to fascicles ) although the artifact obscuring lead I does limit the interpretation.

What happened ?

The patient underwent DC cardioversion under procedural sedation with reversion to sinus rhythm, post cardioversion ECG below.

Post cardioversion

Despite no chest pain the post cardioversion ECG shows infero-lateral ST segment depression with ST elevation in aVR, the patient's troponin peaked at 1.4 [Normal <0.05].

An angiogram was performed which showed:

LAD: 50% Stenosis
Cx: 60% Stenosis
RCA: 30% Stenosis