The normal function of the heart muscle is the result of electro-mechanic and hemodynamic coupling. Modification of the structure and activity of ion channels within the cardiomyocytes may induce cardiac arrhythmias. Electrophysiological mechanisms of arrhythmia, generated by a prolonged period of repolarization, result either from conduction disturbances (reentry mechanism) and/or the induction of beats (early after-depolarizations). Local anaesthetic drug deposition does not affect the repolarization period, as long as the concentration of the free drug in the plasma does not reach the critical value to cause toxic effects in the cardiomyocytes. When analyzing the effect of regional anaesthesia on the repolarization period it is essential to acknowledge the activity or blockade of adrenergic fibres. Blocking the sympathetic fibres', including level T1 to T4, leads to a shortening of the QT interval and a reduction of QT dispersion. Adrenergic blockade as a result of spinal anaesthesia causes severe adrenergic activity above the level of the block and therefore prolongs repolarization. Stellate ganglion block on the right side causes a significant prolongation of the QT interval and QT dispersion. Regardless of the reasons for prolongation of the repolarization period (congenital or acquired), vigilance is required within the perioperative anaesthetic management of a patient, so as not to lead to the occurrence of ventricular arrhythmias. Regional anaesthesia techniques and properly used local anaesthetic drugs are regarded as being safe in these patients.
Keywords: cardiac repolarization; local anaesthetics; long QT syndromes; regional anaesthesia.