Polymorphic Ventricular Tachycardia or Torsades de Pointes?

This is a 60 yo patient admitted due SOB.

Figure 1

It started with a (sinus) narrow QRS rhythm with a Qtc of 485 ms. Then it converted to a wide QRS rhythm with  varying amplitude (height). 

So, someone checked  and found the patient to be unconscious and with no pulse. CPR was initiated and a code was called.

Figure  2

With very good CPR, 1 shock and 1 dose epinephrine the rhythm came back in 10 minutes (perfusing SR).

Is this Torsades de pointes (TdP)? 

Tdp refers to a VT characterized by QRS complexes of changing amplitude that appear to twist around the isolelecttic line and occur at rates of 200-250 bpm. It is characterized by prolonged QT intervals (generally exceeding 500 ms).

There is a less common form of TdP (short-couple variant). This is initiated with a close-coupled PVC and usually does not involve preceding pauses or bradycardia. This is a malignant disease with high mortality and had several characteristics with idiopathic VF.

VT that is similar in morphology to TdP that occurs in patients WITHOUT QT prolongation should generally be classified  as polymorphic VT and not as TdP.

Why make a distinction between TdP and polymorphic VT (similar in morphology to TdP wtihout QT prolongation)? 

This is due to therapeutic implications. In patients with TdP, giving drugs like amiodarone/dofetlide or sotalol can increase the already abnormal QT interval creating more problems. For TdP from acquired causes, magnesium is the initial treatment of choice followed by temporary pacing.

When QT is normal (polynmorphic VT resembling TdP) then standard antiarrhtyhmics can be given. 

So this one was polymorphic VT, the case entered the pulseless VT algorithm and interventions (and the team) did well.

All the electrolytes are in the normal range but the ejection fraction (EF) is about 25%.

Reference:

Bonnow et al. 2011. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 9th Edition. PA.Saunders 

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