The EC₅₀ Of Sufentanil Blunting Cardiovascular Responses To Endobronchial Intubation Combinations With Midazolam And Propofol TCI

Objective: The objective of this study was to determine theeffect-site concentration of sufentanil for suppressing the hemodynamicresponse to endobronchial intubation with the probability of50%(EC50) inpatients receiving midazolam and target controlled infusion of propofolanesthesia by the Dixons up-and-down methods (UDM). Methods: Twenty-oneASA physical status I or II patients, between the ages of18-65, BMI18-25kg/m2, no difficult ventilation and tracheal intubation, who were scheduled forthoracic surgery requiring left endobronchial intubation were recruited into thisstudy. All patients received no premedication. After arrival in the operatingroom, standard monitoring was used throughout the study, which includedelectrocardiography (ECG), heart rate (HR), noninvasive arterial blood pressure(NIBP) and pulse oxymeter(SPO2),18-gauge IV cannulas were placed in leftforearm veins, and10ml/kg/h Ringer’s solution was infused. After10min,midazolam of0.04mg/kg, cisatracurium of0.15mg/kg, propofol of3.5μg/mland sufentanil were administered intravenously for endobronchial intubation.Sufentanil was administered by target-control infusion device. Heart rate(HR),systolic pressure(SBP), diastolic pressure(DBP), mean arterial pressure (MAP)and pulse oxygen saturation(SPO2) were recorded at the following times: T0,baseline (averaged the value of arrival at operation room one minute and fiveminute); T1, at the time of OAA/S≤1; T2, before endobronchial intubation; T3,one minute after endobronchial intubation; T4, three minute after endobronchialintubation; T5, five minute after endobronchial intubation. The Dixon "up-and-down" sequential allocation method was used to determine theeffect-site concentrations of sufentanil. The first patient received an effect-siteconcentration of0.36ng/ml sufentanil. A logarithmic dose interval of0.05wasused. The responses of blocking hemodynamic determined the effect-siteconcentrations of sufentanil given to the next patient. When the sixth turningpoint appeared, the trial was ended. Success or failure of blockinghemodynamic responses was determined by maximal HR and MBP afterendobronchial intubation compared with baseline value. Failure was defined asa patient that showed an increase of either HR or MBP≥20%. The involvedpatients were divided into one of two groups, success or failure, based on theirresponse to the endobronchial intubation. Results:1.There were no significantdifference in gender, age, BIM and ASA physical status between the two groups(P>0.05).2. Basal (T0) HR and MAP did not differ between the two groups(P>0.05). HR and MAP increased significant in failure groups afterendobronchial intubation one minute (T3)(P<0.05), which increased≥20%.HR and MAP in success groups did not increased>20%.3.The EC50ofsufentanil for suppressing the hemodynamic response to endobronchialintubation was0.34ng/ml（0.33-0.36）ng/ml after induction of anesthesia using0.04mg/kg of midazolam and3.5μg/ml of propofol TCI by Dixon and Moodestimator. In Probit analysis, the EC50of sufentanil was0.34ng/ml（0.31-0.37）ng/ml. Conclusion:1. Sufentanil was effective in blunting the cardiovascularresponses to endobronchial intubation, and smaller influence of hemodynam.2.When combined with midazolam0.04mg/ml and target controlled infusion ofpropofol3.5μg/ml, the effect-site concentrations of sufentanil effectiveblunting cardiovascular responses to left endobronchial intubation in50%ofpatients was0.34ng/ml.