Interpretation:
Note: Lead V6 missing – ECG not fully interpretable
Rate: 60bpm – 300bpm
Rhythm: Biphasic p II, III; can be normal. NSR
Axis: normal
P and PR: NSR. PR normal 160ms
Q: pathological Q wave aVF
QRS:
– Have narrow complex QRS 80ms
– Multiple VEB noted
– On rhythm strip, note “R on T” phenomenon – PVC occurs on preceding T wave and results in polymorphic VT
– polymorphic VT: QRS complexes of varying amplitude (difficult to see only on this short portion of ECG but visible on corresponding monitor)
– 6th complex of polymorphic VT also shows a fusion beat
ST/T: no STE/STD. TWI in aVL
QT: Bazett QTC for narrow complex portion of ECG shows QTC of 440ms
Interpretation: patient has R on T phenomenon and evidence of a polymorphic VT. It is NOT Torsades de Pointes as the QTc is normal.
Diagnosis of TdP requires evidence of BOTH polymorphic VT AND QT prolongation.
Questions:
1. Interpret this ECG (as above)
2. How would you treat this patient?
Answers:
2. Management of non-torsades polymorphic VT
- If patient is unstable (shock/syncope/ischaemia/heart failure) —> DCCV
- If patient is stable:
1) Optimise electrolytes – 4g IV MGSO4 over 10mins
Aim Mg 1.5-2mmol
Aim K > 4,5
Correct hypocalcemia
2) Prevention of further episodes: lignocaine or amiodarone (as QT is normal).
3) Treat cause – in most cases of polymorphic non torsades VT –> cause is ischaemia or due to underlying cardiomyopathy.
May require ICD.
This patient:
– Went into cardiac arrest shortly after this episode —> was shocked x 1 and ROSC. Then commenced on Mg and lignocaine. The likely cause was cardiac ischaemia with an underlying cardiomyopathy – LVEF 15%.
References:
Life in the fast lane
EMCRIT
Deranged physiology
Dr Smith’s ECG blog