PROPOFOL HAS NO DIRECT EFFECT ON SINOATRIAL NODE FUNCTION OR ON NORMAL ATRIOVENTRICULAR AND ACCESSORY PATHWAY CONDUCTION IN WOLFF-PARKINSON-WHITE SYNDROME DURING ALFENTANIL MIDAZOLAM ANESTHESIA

Background: Propofol has been implicated as causing intraoperative bra dyarrhythmias. Furthermore, the effects of propofol on the electrophys iologic properties of the sinoatrial (SA) node and on normal atriovent ricular (AV) and accessory pathways in patients with Wolff-Parkinson-W hite syndrome are unknown. Therefore, this study examined the effects of propofol on the cardiac electrophysiologic properties in humans to determine whether propofol promotes bradyarrhythmias and its suitabili ty as an anesthetic agent in patients undergoing ablative procedures. Methods: Twelve patients with Wolff-Parkinson-White syndrome undergoin g radiofrequency catheter ablation were studied. Anesthesia was induce d with alfentanil (50 mu g/kg), midazolam (0.15 mg/kg), and vecuronium (20 mg) and maintained with alfentanil (2 mu g . kg(-1) . min(-1)) an d midazolam (1-2 mg, every 15 min, as needed). A electrophysiologic st udy was performed consisting of measurement of the effective refractor y period of the right atrium, AV node, and accessory pathway and the s hortest cycle length of the AV node and accessory pathway during anteg rade stimulation plus the effective refractory period of the right ven tricle and accessory pathway and the shortest cycle length of the acce ssory pathway during retrograde stimulation. Determinants of SA node f unction including sinus node recovery time, corrected sinus node recov ery time, and SA conduction time; intraatrial conduction time and atri al-ais Interval also were measured, Reciprocating tachycardia was indu ced by rapid right atrial or ventricular pacing, and the cycle length and atrial-His, His-ventricular, and ventriculoatrial intervals were m easured, Alfentanil/midazolam was then discontinued, Propofol was admi nistered (bolus 2 mg/kg + 120 mu g . kg(-1) . min(-1)), and the electr ophysiologic measurements were repeated. Results: Propofol caused a st atistically significant but clinically unimportant prolongation of the right atrial refractory period. The effective refractory periods of t he AV node, right ventricle, and accessory pathway, as well as the sho rtest cycle length, were not affected. Parameters of SA node function and intraatrial conduction also were not affected. Sustained reciproca ting tachycardia was inducible in 8 of 12 patients, and propofol had n o effect on its electrophysiologic properties. All accessory pathways were successfully identified and ablated. Conclusions: Propofol has no clinically significant effect on the electrophysiologic expression of the accessory pathway and the refractoriness of the normal AV conduct ion system. In addition, propofol has no direct effect on SA node acti vity or intraatrial conduction; therefore, it does not directly induce bradyarrhythmias. It is thus a suitable agent for use in patients und ergoing ablative procedures who require either a neuroleptic or genera l anesthetic.