Torsades de Pointes

Torsade de Pointes

Physiology

  • Ventricular repolarisation is initiated by exodus of intracellular K+.
  • Drugs can block this K+ channel - delaying repolarisation (prolonging Q-T interval).
  • Other factors are
    • Female
    • ↑ Age
    • Electrolyte disturbance CCF, Bradycardia, Ischaemia Congenital Main drug culprits listed below
Torsade de Pointes rhythm strip - Thank you Dr. Peter Kearney
Rhythm strip courtesy Dr Peter Kearney

Causes

  • Antiarrhythmics especially Class Ia and III.
  • Phenothiazines and butyrophenones.
  • Tricyclic antidepressants.
  • Nonsedative antihistamines.
  • Some antibiotics especially macrolides and antifungals.
  • Organophosphates.
  • Cocaine
  • Electrolyte abnormalities (hypokalaemia, hypomangesemia)
  • SAH

 

Treatment

TdP

Aim of treatment in TdP :

  1. To treat haemodynamic compromise immediately.
  2. To alter the afterdepolarisation effect.
  3. To shorten the QT interval.
  1. Haemodynamic compromise requires immediate DC cardioversion. (Synchronised 200, 200, 360J)
  2. 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.
  3. Correction of hypokalaemia to a serum K+ concentration of > 4.5 mmol/l also helps suppress EAD`s.
  4. Lignocaine has been used.
    1. However its effect is inconsistent with a reported success rate of only 50%.
  5. 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 repolarisation duration.
  6. Isoprenaline should only be a temporising measure as in can promote EAD`s.
  7. Involve a cardiologist early.