The influence of regional anaesthesia and local anaesthetics on cardiac repolarization

Abstract

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.Key words: long QT syndromes, cardiac repolarization, regional anaesthesia, local anaesthetics Anaesthesiology Intensive Therapy 2016, vol. 48, no 2, 135-141 CARDIAC ELECTROPHYSIOLOGYNormal function of the heart muscle is the result of electro-mechanic and haemodynamic coupling. When considering cardiac electrical activity from the point of view of a working myocardial cell, the following must be acknowledged: the relaxed state (polarization of the cell membrane) and active state (depolarization-repolarization) occurring after activation by the conduction system. Changes in the phases of action potential and the resting potential are the result of a synchronized movement of ionic currents through the ion channels, pumps and cardiomyocyte cell membrane carriers. The period of depolarization is initiated by an inward sodium current (I Na ), supported by an inward calcium current (I Ca-L ). During repolarization the flow of current occurs through the channels conducting the potassium current (I Kr , I Ks , I to , I K (ATP) ) and to a lesser extent by the sodium current (I Na ), calcium current (I Ca-L ) and non-selective cation channel (I NS ). This is depicted in Figure 1.The intracellular influx of calcium ions during the plateau phase enables a calcium dependent calcium release from the sarcoplasmic reticulum, leading to a contraction of the working myocardial cell. Under such physiological conditions during repolarization, potassium I Kr and I Ks...

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“…28 One more explanation for bradycardia, could be related with the effects of a local anaesthetic on sodium channels in the heart that results in depolarisation reduction. 31…”