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The QT interval, which is measured from the start of the Q wave (or the R wave when no Q wave is present) to the completion of the T wave, reflects the duration of electrical ventricular systole. The duration of systole varies with heart rate and therefore the measured QT interval is often corrected for heart rate using the following formula, in which QTc represents the rate corrected value: QTc = Qt/VRR interval The QTc interval is normally less than 440 ms [1]. Increased serum concentrations of noradrenaline and a change in the balance between sympathetic and parasympathetic tone may be associated with prolonged QT interval [2, 3]; this may be controlled with either f}-block [4] or stellate ganglion block [5]. Hypomagnesaemia and, more commonly, hypokalaemia cause clinically significant prolongation which may be produced by effects on the repolarizing potassium current. Sleep (which is associated with a reduction in sympathetic tone) prolongs QTc [6]. Induction of anaesthesia with thiopentone prolongs significantly the QT interval [7], whereas Althesin had no effect [8]. The most marked changes follow tracheal intubation facilitated with suxamethonium, but these changes may be reduced by pretreatment with tubocurarine [7] or by (3-block [9], suggesting mediation by the sympathetic nervous system. It has been reported also that the QT interval is significantly prolonged by enflurane [8, 10], but not by halothane anaesthesia [8]. The mechanism underlying these differences has not been explained. It has been reported that these volatile agents and also

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