Note: Lead V6 missing – ECG not fully interpretable
Rate: 60bpm – 300bpm
Rhythm: Biphasic p II, III; can be normal. NSR
P and PR: NSR. PR normal 160ms
Q: pathological Q wave aVF
– 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.
1. Interpret this ECG (as above)
2. How would you treat this patient?
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
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.
– 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%.
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Dr Smith’s ECG blog