Background
- Torsade de pointes ( TdP ) is a form of polymorphic ventricular pro-arrhythmia
- Associated with QT interval prolongation and prominent U waves on resting ECG
- ECG = prolonged re-polarisation and so, early after depolarisation (EAD)
- Can be congenital
- Usually acquired due to potassium channel dysfunction
- It may degenerate to VF
Physiology
- Ventricular re-polarisation is initiated by exodus of intracellular K+
- Drugs can block this K+ channel - delaying re-polarisation (prolonging Q-T interval)
- Other factors are:
- Female
- ↑ Age
- Electrolyte disturbance CCF, Bradycardia, Ischaemia Congenital Main drug culprits listed below
(Drug) Causes
- Antiarrhythmics especially Class Ia and III
- Phenothiazines and butyrophenones
- Tricyclic antidepressants
- Non-sedative antihistamines
- Some antibiotics especially macrolides and anti-fungals
- Organophosphates
- Cocaine
- Electrolyte abnormalities (hypokalaemia, hypomangesaemia)
- SAH
Treatment
Aim of treatment in TdP :
- To treat haemodynamic compromise immediately
- To alter the after-depolarisation effect
- To shorten the QT interval
- Haemodynamic compromise requires immediate DC cardioversion. (Synchronised 150-200J)
- Magnesium, at a dose of 2g magnesium sulphate intravenously over one to two minutes, is used to suppress EAD`s in the emergency situation. The serum magnesium level need not be known prior to treatment
- Correction of hypokalaemia to a serum K+ concentration of > 4.5 mmol/l also helps suppress EAD`s
- Lignocaine has been used:
- However its effect is inconsistent with a reported success rate of only 50%
- Cardiac pacing at 100-140/min is the treatment of choice. The basic heart rate should be accelerated, as there is an inverse relationship between rate and the re-polarisation duration
- Isoprenaline should only be a temporising measure as in can promote EADs
- Involve a cardiologist early