Wednesday, 22 January 2014

ECG of the Week - 20th January 2014 - Interpretation

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
  • VT 
    • 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


    The patient underwent a cardiac ablation following this episode.


    References / Further Reading

    Life in the Fast Lane

    Textbook
    • Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.