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Background: Propofol has been implicated as causing intraoperative bradyarrhythmias. Furthermore, the effects of propofol on the electrophysiologic properties of the sinoatrial (SA) node and on normal atrioventricular (AV) and accessory pathways in patients with Wolff-Parkinson-White 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 suitability as an anesthetic agent in patients undergoing ablative procedures., Methods: Twelve patients with Wolff-Parkinson-White syndrome undergoing radiofrequency catheter ablation were studied. Anesthesia was induced with alfentanil (50 micrograms/kg), midazolam (0.15 mg/kg), and vecuronium (20 mg) and maintained with alfentanil (2 micrograms.kg-1.min-1) and midazolam (1-2 mg, every 15 min, as needed). A electrophysiologic study was performed consisting of measurement of the effective refractory period of the right atrium, AV node, and accessory pathway and the shortest cycle length of the AV node and accessory pathway during antegrade stimulation plus the effective refractory period of the right ventricle and accessory pathway and the shortest cycle length of the accessory pathway during retrograde stimulation. Determinants of SA node function including sinus node recovery time, corrected sinus node recovery time, and SA conduction time; intraatrial conduction time and atrial-His interval also were measured. Reciprocating tachycardia was induced by rapid right atrial or ventricular pacing, and the cycle length and atrial-His, His-ventricular, and ventriculoatrial intervals were measured. Alfentanil/midazolam was then discontinued. Propofol was administered (bolus 2 mg/kg + 120 micrograms.kg-1.min-1), and the electrophysiologic measurements were repeated., Results: Propofol caused a statistically significant but clinically unimportant prolongation of the right atrial refractory period. The effective refractory periods of the AV node, right ventricle, and accessory pathway, as well as the shortest cycle length, were not affected. Parameters of SA node function and intraatrial conduction also were not affected. Sustained reciprocating tachycardia was inducible in 8 of 12 patients, and propofol had no 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 conduction system. In addition, propofol has no direct effect on SA node activity or intraatrial conduction; therefore, it does not directly induce bradyarrhythmias. It is thus a suitable agent for use in patients undergoing ablative procedures who require either a neuroleptic or general anesthetic.

Background: The effects of volatile agents and sufentanil anesthesia on the electrophysiologic properties of the accessory pathway and on the incidence of intraoperative tachyarrhythmias in patients with Wolff-Parkinson-White syndrome are unknown. Therefore, we studied these agents for their use in patients undergoing ablative procedures or requiring a general anesthetic for other surgeries., Methods: Twenty-one patients with Wolff-Parkinson-White syndrome undergoing surgical ablation were anesthetized with sufentanil (20 micrograms/kg), lorazepam (0.06 mg/kg), and vecuronium (20 mg). After sternotomy, the electrophysiologic study during antegrade stimulation consisted of the effective refractory period of the right atrium, atrioventricular node, and accessory pathway; the shortest cycle length of the atrioventricular node and accessory pathway; and the coupling interval. During retrograde stimulation, the effective refractory period of the right ventricle and accessory pathway and the shortest cycle length of the accessory pathway were measured and compared to preoperative electrophysiologic values. Patients then were randomized to receive 1 MAC of halothane, isoflurane, or enflurane, and the electrophysiologic study was repeated., Results: Sufentanil-lorazepam caused mild prolongation (P < 0.05) of the effective refractory period of the accessory pathway and the shortest cycle length of the atrioventricular node. Enflurane and isoflurane significantly prolonged all parameters related to refractoriness during antegrade conduction, with enflurane having the largest effect. During retrograde conduction, isoflurane prolonged the effective refractory period of the right ventricle and accessory pathway and the shortest cycle length of the accessory pathway, whereas enflurane prolonged only the accessory pathway effective refractory period and shortest cycle length. Halothane had the least effect on refractoriness, causing significant prolongation of the atrioventricular node effective refractory period and the shortest cycle length of the accessory pathway only during antegrade conduction. The coupling interval, a measure of the period of vulnerability to supraventricular tachycardia, was prolonged only by halothane and isoflurane. Supraventricular tachycardia was still obtainable in all patients., Conclusions: Sufentanil-lorazepam has no clinically significant effect on the electrophysiologic expression of the accessory pathway. Of the volatile agents, enflurane most, isoflurane next, and halothane least increased refractoriness within the accessory and atrioventricular pathways. Therefore, administration of these volatile agents during ablative procedures may confound interpretation of postablative studies used to determine the success of ablation treatment. Conversely, in patients with preexcitation syndrome requiring general anesthesia for nonablative procedures, volatile agents may reduce the incidence of perioperative tachyarrhythmias because of their effects on refractoriness. Enflurane would be the agent of choice because it increases refractoriness the most without prolonging the coupling interval.

The effects of alfentanil-midazolam anaesthesia upon the electrophysiologic (EP) properties of normal atrioventricular (A-V) and accessory pathway (AP) conduction were studied in eight patients with Wolff-Parkinson-White syndrome during accessory pathway surgical ablation. The presence of an AP was confirmed by preoperative EP studies. Anaesthesia was induced with alfentanil (50 micrograms.kg-1) and midazolam (0.15 mg.kg-1) and maintained with an alfentanil infusion (2 micrograms.kg-1.min-1) and intermittent boluses of midazolam (1-2 mg q 15 min, PRN). Following sternotomy, a baseline EP study was performed which consisted of effective refractory period (ERP) and shortest cycle length (SCC) measurement during antegrade conduction in the AV and AP, as well as during retrograde conduction in the AP. Comparison with preoperative EP studies indicated that the administration of alfentanil-midazolam anaesthesia had no effect upon conduction or ERP in either pathway. Haemodynamic stability occurred throughout the surgical procedure with no tachyarrhythmias. We conclude that a combination of alfentanil-midazolam is suitable for general anaesthesia in patients undergoing ablative procedures for accessory pathways.