The effect of intravenous labetalol administration on hemodynamic responses during desflurane inhalation.

Abstract

BackgroundInspired concentrations of desflurane ≥ 1 minimum alveolar anesthetic concentration (MAC) have been related to sympathetic stimulation such as hypertension and tachycardia. The current study examined whether labetalol, an α1 and β-adrenergic antagonist would blunt these hemodynamic responses.MethodsFifty-four ASA physical status I patients, aged 20-60 years, were enrolled in this study. The patients were randomly divided into 2 groups. The breathing circuit was primed with an end-tidal desflurane concentration of 1.2 MAC in 6 L/min O2. Normal saline 5 ml or labetalol 0.3 mg/kg was injected into groups S and L respectively. After 5 minutes, anesthesia was induced with intravenous etomidate 0.2 mg/kg and vecuronium 0.1 mg/kg. Each patient inhaled desflurane through a tight fitting facemask. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and end-tidal concentration of desflurane (et-des) were measured at 5 minutes after saline or labetalol injection (baseline) and every 1 minute for 5 minutes after desflurane inhalation and for 2 minutes after intubation.ResultsIn the saline injection group (group S), desflurane inhalation increased heart rate and blood pressure, while labetalol 0.3 mg/kg attenuated the heart rate and blood pressure increase in group L. After tracheal intubation, heart rate and blood pressure were significantly lower in group L than in group S.ConclusionsThese results demonstrate that administration of intravenous labetalol is effective in attenuating tracheal intubation and desflurane-induced hemodynamic responses.