Midazolam premedication reduces propofol dose requirements for multiple anesthetic endpoints

PURPOSE: This study investigates the interactions between midazolam premedication and propofol infusion induction of anesthesia for multiple anesthetic endpoints including: loss of verbal contact (LVC; hypnotic), dropping an infusion flex (DF; motor), loss of reaction to painful stimulation (LRP; antinociceptive) and attainment of electroencephalographic burst suppression (BUR; EEG). METHODS: In a double blind, controlled, randomized and prospective study, 24 ASA I-II patients received either midazolam 0.05 mg x kg(-1) (PM; n = 13) or saline placebo (PO; n = 11) i.v. as premedication. Twenty minutes later, anesthesia was induced by propofol infusion at 30 mg x kg(-1) x hr(-1). ED50, ED95 and group medians for times and doses were determined and compared at multiple anesthetic endpoints. RESULTS: At the hypnotic, motor and EEG endpoints, midazolam premedication significantly and similarly reduced propofol ED50 (reduction: 18%, 13% and 20% respectively; P <0.05 vs unpremedicated patients) and ED95 (reduction: 20%, 11% and 20% respectively; P <0.05 vs unpremedicated patients). For antinociception (LRP), dose reduction by premedication was greater for propofol ED95 (reduction: 41%; P <0.05 vs unpremedicated patients) than ED50 (reduction: 18%; P <0.05 vs unpremedicated patients). Hemodynamic values were similar in both groups at the various endpoints. CONCLUSIONS: Midazolam premedication 20 min prior to induction of anesthesia reduces the propofol doses necessary to attain the multiple anesthetic endpoints studied without affecting hemodynamics in this otherwise healthy population. The interaction differs for different anesthetic endpoints (e.g., antinociception vs hypnosis) and propofol doses (e.g., ED50 vs ED95).     

Midazolam coinduction does not delay discharge after very brief propofol anaesthesia

Previous reports have demonstrated synergism of midazolam and propofol for induction of anaesthesia in humans. We tested the hypothesis that in the presence of alfentanil, the combination of midazolam with propofol for a very brief operative procedure would not affect the recovery phase. During pre-oxygenation, 64 outpatients scheduled for dilatation and curettage received placebo, or low-dose midazolam (0.03 mg · kg^?1), or high-dose midazolam (0.06 mg · kg^?1) iv, in a randomized double-blind manner. They then received alfentanil 10 μg · kg^?1 iv, followed by titrated doses of propofol iv for induction and maintenance of anaesthesia. Ventilation with 70% N₂O in O₂ by mask was controlled to achieve a PETCO₂ 30–40 mmHg. Outcome measures were: propofol dose (induction and maintenance), time until eye-opening to command, and time to discharge-readiness. Propofol induction dose was decreased by increasing doses of midazolam (P = 0.00005). Midazolam delayed time to eye-opening (P = 0.02) but not time to discharge-readiness. This study had an 80% power to detect a 39 min difference in time to discharge-readiness. We conclude that midazolam propofol co-induction in the presence of alfentanil delays eye-opening, but does not delay discharge after anaesthesia.     

Cardiovascular effects of sedative infusions of propofol and midazolam after spinal anaesthesia

The cardiovascular effects of intravenous sedation were studied in fifty patients after spinal anaesthesia for lower limb or pelvic surgery. Twenty patients received propofol (mean dosage 74 (SD 4) micrograms/kg/min for 0-20 minutes and 51 (SD 7) micrograms/kg/min for 20-40 minutes), twenty received midazolam (35 micrograms/kg + 2.54 (SD 0.2) micrograms/kg/min for 0-20 minutes and 1.35 (SD 0.2) micrograms/kg/min for 20-40 minutes) and ten patients received saline infusion only. The forearm vasoconstriction in response to the spinal anaesthesia was measured by strain gauge plethysmography. Spinal anaesthesia lowered systolic and diastolic blood pressure by 18 (SED 4) mmHg and 9 (SED 2) mmHg respectively. (SED = standard error of the difference.) This was associated with a 32% decrease in mean forearm blood flow. Propofol and midazolam caused similar additional reductions in systolic and diastolic blood pressure (10 (SED 4) mmHg and 4 (SED 2) mmHg) and a decrease in heart rate (P less than 0.005), but forearm vasoconstriction was not altered. In the control group, however, forearm vasoconstriction increased during 40 minutes in theatre (P less than 0.05). Recovery from propofol was far more rapid than after midazolam and was virtually complete in ten minutes. This was reflected by an increase in blood pressure and in forearm vasoconstriction in the recovery period.     

Efficacy of ketamine and midazolam as co-induction agents with propofol for laryngeal mask insertion in children

Objectives: Use of midazolam and ketamine lowers the induction dose of propofol (co‐induction) producing hemodynamic stability. Background: Large doses of propofol needed for induction and laryngeal mask (LM) insertion in children may be associated with hemodynamic and respiratory effects. Co‐induction has the advantage of reducing dose and therefore maintaining hemodynamic stability. Aim: To examine the effect of co‐induction on hemodynamics, LM insertion and recovery in children. Methods/Materials: A prospective, randomized, double‐blind, controlled study was conducted in 60 ASA I/II children, age 1–8 years. Normal saline, ketamine 0.5 mg·kg^?1, midazolam 0.05 mg·kg^?1 were administered in groups P (propofol), PK (propofol–ketamine) and PM (propofol–midazolam), respectively, 2 min prior to the administration of the induction dose of propofol. Propofol 3.5 mg·kg^?1 (group P) or 2.5 mg·kg^?1 (groups PK and PM) was used for induction, LM inserted 30 s later and insertion conditions assessed. Heart rate and blood pressure were recorded immediately after propofol bolus, then every min till 2 min after LMA insertion. Recovery was assessed using Steward’s Score. Result: In group P, systolic blood pressure (SBP) showed a significantly greater decrease compared to group PK and group PM (P < 0.005). Only 5% of patients in groups PK and PM showed >20% fall in SBP compared to 89% in group P (P < 0.005). More children in groups PK and PM had acceptable conditions for LM insertion compared to group P (P < 0.05). The time to achieve Steward Score of 6 was longer in groups PK and PM compared to group P (P < 0.005). Conclusion: In children, the combination of propofol with ketamine or midazolam produces stable hemodynamics and improved LM insertion conditions but is associated with delayed recovery.     

不同剂量咪达唑仑与异丙酚催眠效应的相互作用

目的 评价不同剂量咪达唑仑与异丙酚催眠效应的相互作用.方法 择期全麻病人120例,ASA Ⅰ或Ⅱ级,年龄18～60岁,体重40～80 kg,随机分为4组(n=30),各组分别随机分为6个亚组,M组和P组各亚组分别静脉注射咪达唑仑0.04、0.06、0.08、0.10、0.12、0.15 mg/kg、异丙酚0.8、1.0、1.2、1.5、1.8、2.2 mg/kg;MP1组和MP2组各亚组分别按咪达唑仑与异丙酚ED50等效比1:13(咪达唑仑剂量分别为0.022、0.028、0.033、0.039、0.044、0.055 mg/kg)和临床常用比例1:10(咪达唑仑剂量分别为0.03、0.04、0.045、0.05、0.055、0.06 mg/kg)行麻醉诱导.M组、P组、MP1组和MP1组分别于注药后3、1,1、1 min时行警觉,镇静(OAA/S)评分,催眠有效标准:OAA/S评分≤2分.采用加权概率单位法计算半数有效剂量(ED50)及其95%可信区间(95%CI);采用等辐射分析法判断两药催眠效应的相互作用.结果 M组、MP1.2组咪达唑仑催眠效应的ED50及其95%CI分别为0.088(0.066～0.110)、0.031(0.026～0.036)、0.045(0.040～0.049)mg/kg;P组、MP1.2组异丙酚催眠效应的ED50及其95%CI为1.142(0.933～1.350)、0.421(0.343～0.480)、0.450(0.399～0.491)mg/kg.结论 麻醉诱导时咪达唑仑与异丙酚按ED50等效剂量比1:13给药,两药催眠效应为协同作用;按临床常用剂量比1:10给药时两药催眠效应为相加作用.     

Implantable cardioverter-defibrillator placement in patients with mild-to- moderate left ventricular dysfunction: hemodynamics and recovery profile with two different anesthetics used during deep sedation

OBJECTIVE: To compare the effects of thiopental and propofol during defibrillation threshold testing (DFT) on hemodynamics and recovery profile in patients requiring automatic internal cardioverter-defibrilator placement. DESIGN: Prospective clinical investigation. SETTING: University hospital. PARTICIPANTS: Thirty-four adult patients. INTERVENTIONS: After administration of midazolam, 0.025 mg/kg, and fentanyl, 0.5 to 1 mug/kg, surgery was performed under topical infiltration with 1% lidocaine. In group I (GI) (n = 17), patients received thiopental by slow injection and patients in group II (GII) (n = 17) received propofol before induction of ventricular fibrillation (VF). MEASUREMENTS AND MAIN RESULTS: Patients received 4.1 +/- 1.4 mg of midazolam, 114 +/- 34 mug of fentanyl, and 280 +/- 78 mg of thiopental in GI; and 4.6 +/- 1.7 mg of midazolam, 119 +/- 62 mug of fentanyl, and 147 +/- 40 mg of propofol in GII (p > 0.05). Hemodynamics did not show significant differences between the groups at any recording time. Average time needed to regain the pretest sedation level was 16.4 +/- 8.8 minutes in GI and 10.9 +/- 5.5 minutes in GII (p = 0.03). Time required to achieve a score of 10 using a modified Aldrete score was 26.4 +/- 9.3 minutes in GI and 17.4 +/- 4.9 in GII (p = 0.001). Seven patients in GII (41%) and 1 patient in GI (6%) became hypotensive after DFT (p = 0.04). CONCLUSIONS: Deepening the sedation level by slow injection of thiopental or propofol before DFT provided satisfactory conditions during brief episodes of VF. Delay in recovery of arterial pressure after DFT with propofol and delay in arousal and discharge of patients with thiopental are major disadvantages of the regimens.     

Prilocaine reduces injection pain caused by propofol

Propofol, which is commonly used for outpatient anaesthesia, may evoke pain during infusion. Forty-eight patients (ASA I-II) undergoing elective uterine dilatation and curettage received randomly in a standardised fashion: A: Propofol mixed with prilocaine; B: Propofol and lidocaine; C: Propofol with prilocaine + lidocaine (equal amounts) or D: Propofol and saline. The final ratio of propofol: local anaesthetic/saline was 9: 1 in all mixtures. Pain on injection was significantly decreased in the three groups receiving propofol and local anaesthetic(s) compared to the one given propofol and saline. Propofol is required in greater amounts when mixed with lidocaine than when mixed with saline. A binding between the algesic part of the propofol molecule and the local anaesthetic agent may explain these findings. Another twenty-two comparable patients were given 30 mg of ketorolac or an equal volume of saline intramuscularly 45 60 minutes prior to propofol. Ketorolac given before propofol did not reduce pain on injection. This indicates that inhibition of the cyclooxygenase pathway of arachidonic acid metabolism does not play a major role in the reduction of this pain.     

Propofol auto-co-induction as an alternative to midazolam co-induction for ambulatory surgery

We propose the use of an intravenous propofol/propofol auto-co-induction technique as an alternative to propofol/midazolam for induction of anaesthesia. We have studied 54 unpremedicated ASA 1 or 2 patients undergoing day-stay anaesthesia for minor orthopaedic surgery. All received 10 micrograms.kg-1 or alfentanil before induction, followed by either midazolam 0.05 mg.kg-1, propofol 0.4 mg.kg-1 or saline, and 2 min later, a propofol infusion at a rate of 50 mg.kg-1.h-1 until loss of eyelash reflex. We compared pre- and postinduction haemodynamic changes, complications at insertion of a laryngeal mask airway and recovery from anaesthesia in the three groups. Both co-induction techniques showed less postinduction hypotension and significant reduction of the total induction dose of propofol when compared to the control group. In the propofol/propofol group there was a decreased incidence of apnoea during induction of anaesthesia. These patients were discharged from hospital 2 h after the end of anaesthesia whereas patients in the midazolam/propofol group were discharged after 2 1/2 h (p < 0.001).     

咪唑安定与丙泊酚对脑电双频指数的影响

目的测定和比较咪唑安定与丙泊酚诱导时半数病人入睡时的脑电双频指数（BIS50）和半数有效量（ED50）。方法选择60例无服用精神药物和镇静催眠药物史、无术前用药的门诊手术病人（ASAⅠ～Ⅱ级），随机均分为咪唑安定组（M组）和丙泊酚组（P组），以半数效量序贯法分别进行咪唑安定与丙泊酚诱导的睡眠观察，以对语言指令和睫毛反射消失为入睡指标，同时记录BIS的变化。对取得的数据以直线回归的方法和加权均数法分别求得咪唑安定、丙泊酚的BIS50和ED50。结果咪唑安定诱导后，术峤病人与入睡病人的BIS值均较用药前的基础值明显下降，但下降幅度在两类病人之间差异无统计学意义，BISso和EDso分别为：77．02（95％可信区间为：71．08～85．86）和0．1237mg／kg（95％可信区间为：0．0990-0．1540mg／kg）。丙泊酚诱导时未睡病人的BIS值下降不明显，而入睡病人的BIS值显著下降，两者之间差异有统计学意义（P〈0．05）。丙泊酚的BIS50和ED50分别是79．17（95％可信区间为：72．08～88．55）和1．0192mg／kg（95％可信区间为：0．9400～1．1480mg／kg）。结论咪唑安定和丙泊酚对BIS的影响有较大的差异。与丙泊酚比较，BIS值与咪唑安定催眠效果的相关性小于丙泊酚。     

Propofol and midazolam inhibit gastric emptying and gastrointestinal transit in mice

We studied the effect of propofol and midazolam on gastric emptying and gastrointestinal transit in mice. Ten minutes after intraperitoneal injection of propofol or midazolam, 0.2 mL of saline containing fluorescent microbeads was infused into the stomach. Thirty minutes later, the gastrointestinal tract was excised, and gastric emptying and gastrointestinal transit were calculated by measuring the quantity of fluorescent microbeads in the gastrointestinal tract by using a flow cytometer. At a dose that produced a light level of sedation (mice righted themselves within 2 s), both drugs significantly, but weakly, inhibited gastric emptying to a similar degree (propofol: P < 0.001 versus control value; 95% confidence interval [CI] for difference, 4.9%-20.2%; midazolam: P < 0.001 versus control value; 95% CI for difference, 7.8%-14.7%). Midazolam, but not propofol, delayed gastrointestinal transit (P < 0.001). At a larger dose that produced a deeper level of sedation (absence of righting reflex >10 s), both drugs significantly inhibited gastric emptying (propofol: P < 0.001; 95% CI for difference, 31.4%-61.2%; midazolam: P < 0.001; 95% CI for difference, 30.8%-61.1%) and gastrointestinal transit (P < 0.001 for both drugs).     

A comparison of sevoflurane, target-controlled infusion propofol, and propofol/isoflurane anesthesia in patients undergoing carotid surgery: a quality of anesthesia and recovery profile

In a prospective randomized study in patients undergoing carotid endarterectomy, we compared the hemodynamic effects, the quality of induction, and the quality of recovery from a hypnotic drug for the induction of anesthesia with sevoflurane, a target-controlled infusion (TCI) of propofol, or propofol 1.5 microg/kg followed by isoflurane. All patients were premedicated with midazolam and received sufentanil 0.4 microg/kg at induction. The induction of anesthesia was associated with a decrease in arterial blood pressure in all groups, but this was least pronounced in the Sevoflurane group. There were similar a number of episodes of hypotension, hypertension, and tachycardia among groups, but the incidence of bradycardia was less in the TCI group (P < 0.05) compared with the other groups. The duration of episodes of hypotension was shorter (P < 0.05) in the TCI Propofol group (1.9 +/- 2.3 min) compared with the Sevoflurane group (4.7 +/- 3.6 min). The duration of episodes of bradycardia was significantly lower (P < 0.05) in the TCI Propofol group (0.1 +/- 0.5 min) in comparison with the Propofol Bolus group (2.5 +/- 3.9 min). Similar doses of vasoactive drugs were used in all groups. The induction of anesthesia with sevoflurane was associated with inferior conditions for intubation in comparison with both Propofol groups, although the time to intubation was faster in the Sevoflurane group (P < 0.05). The recovery characteristics were similar in the three groups.     

Target-controlled propofol requirements at induction of anaesthesia: effect of remifentanil and midazolam

BACKGROUND AND OBJECTIVE: Target-controlled infusions of anaesthetic agents have become increasingly available. They can involve the use of propofol in combination with an opioid or a benzodiazepine. The effect site concentration of propofol infusions has been advocated as a method of estimating drug distribution. We investigated the influence of co-induction with remifentanil and midazolam on effect site propofol requirements at induction of anaesthesia using target-controlled infusions. METHODS: Sixty-six consenting adult patients were randomly allocated to three treatment groups. Each group received induction of anaesthesia with a different total intravenous technique. One group was induced with target-controlled propofol alone; another received target-controlled propofol and target-controlled remifentanil (3 ng mL-1); and the last received midazolam (0.03 mg kg-1), target-controlled remifentanil (3 ng mL-1) and target-controlled propofol. Computer simulation was used to calculate effect site concentrations. We recorded propofol dose and effect site concentration at loss of verbal response. RESULTS: The effect site concentration (Ce50) of propofol alone was 2.19 micrograms mL-1. This was reduced to 1.55 micrograms mL-1 during co-induction with remifentanil and further reduced to 0.64 microgram mL-1 with midazolam premedication (P < 0.001; ANOVA). CONCLUSIONS: We conclude that co-induction with remifentanil alone or with midazolam can be used to reduce propofol doses at induction of anaesthesia using target-controlled infusions. We believe that using effect site concentration may prove a useful tool in routine clinical practice.     

Effect of midazolam pretreatment on induction dose requirements of propofol in combination with fentanyl in younger and older adults

In a double-blind, randomised trial, we compared the effects of pretreatment with midazolam at two different doses (0.025 and 0.05 mg x kg(-1)), with placebo, on the induction dose requirements of propofol in two different age groups. We enrolled 120 patients: 60 younger patients (aged 18-35 years) and 60 older patients (aged over 60 years). All patients received 0.75 microg x kg(-1) of fentanyl, plus a blinded pretreatment with either saline or one of two doses of midazolam. Induction continued with a fixed rate infusion of propofol. Propofol dose requirement was recorded, as were cardiovascular parameters and the occurrence of significant apnoea (> 60 s). Midazolam pretreatment was associated with a significant reduction in propofol dose requirement in both younger and older patients. The reduction in older patients was significantly greater than the equivalent response in younger groups. There was no demonstrable benefit in terms of improved cardiovascular stability or reduction in the incidence of apnoea. Caution is advised in the use of midazolam as an agent for co-induction with propofol in the elderly.     

Metoclopramide does not influence the frequency of propofol-induced spontaneous movements

STUDY OBJECTIVE: To evaluate the effects of metoclopramide on the frequency and severity of propofol-induced movements. DESIGN: Randomized, double blind, placebo-controlled trial. SETTING: Veterans Administration Medical Center. PATIENTS: One hundred thirty-seven consenting adults scheduled to receive general anesthesia with propofol induction. INTERVENTIONS: Patients were randomized to receive either metoclopramide 10 mg intravenously (IV) or placebo (saline) 3 min before induction of general anesthesia. All patients received midazolam 1 to 2 mg IV, fentanyl 50 to 150 microg IV, and lidocaine 50 to 80 mg IV before induction of anesthesia. MEASUREMENTS: Occurrence of spontaneous movements and severity during the observation period were recorded after propofol induction by observing movement in the hands/arms and feet/legs, as well as presence of a hiccup. The dosage of anesthetic medications administered was also recorded for each patient. MAIN RESULTS: No differences were noted in the frequency and severity of spontaneous movement in the patients who had received metoclopramide and placebo. However, compared with the patients who did not move, patients who experienced movements received a significantly higher dose of propofol (P = 0.025) and a lower dose of fentanyl (P = 0.049). CONCLUSIONS: Metoclopramide does not affect the frequency of propofol-induced movements, but propofol and fentanyl doses influence the frequency of movements during propofol induction.     

Cardiovascular Responses during Sedation after Coronary Revascularization: Incidence of Myocardial Ischemia and Hemodynamic Episodes with Propofol Versus Midazolam

Background: Propofol sedation offers advantages for titration and rapid emergence in the critically ill patient, but concern for adverse hemodynamic effects potentially limits its use in these patients. The current study compares the cardiovascular effects of sedation with propofol versus midazolam during the first 12 h after coronary revascularization.

Methods: Three hundred fifty-one patients undergoing coronary revascularization were anesthetized using a standardized sufentanil/midazolam regimen, and assigned randomly to 12 h of sedation with either propofol or midazolam while tracheally intubated. The incidence and characteristics of hemodynamic episodes, defined as heart rate less than 60 or greater than 100 beats/min or systolic blood pressure greater than 140 or less than 90 mmHg, were determined using data electronically recorded at 1-min intervals. The presence of myocardial ischemia was determined using continuous three-channel Holter electrocardiography (ECG) and of myocardial infarctions (MI) using 12-lead ECG (Q wave MI, Minnesota Code) or creatine kinase isoenzymes (CK-MB) analysis (non-Q wave MI, peak CK-MB > 70 ng/ml, or CK-MB > 70 IU/l).

Results: Ninety-three percent of patients in both treatment groups had at least one hemodynamic episode during the period of postoperative sedation. Propofol sedation resulted in a 17% lower incidence of tachycardia (58% vs. 70%, propofol vs. midazolam; P = 0.04), a 28% lower incidence of hypertension (39% vs. 54%; P = 0.02), and a greater incidence of hypotension (68% vs. 51%; P = 0.01). Despite these hemodynamic effects, the incidence of myocardial ischemia did not differ between treatment groups (12% propofol vs. 13% midazolam; P = 0.66), nor did its severity, as measured by ischemic minutes per hour monitored (8.7+/-5.8 vs. 6.2+/-4.6 min/h, propofol vs. midazolam; P = 0.19) or ischemic area under the curve (6.8+/-4.0 vs. 5.3+/-4.2; P = 0.37). The incidence of cardiac death (one per group), Q wave MI (propofol, n = 7; midazolam, n = 3; P = 0.27), or non Q wave MI (propofol, n = 16; midazolam, n = 18; P = 0.81) did not differ between treatment groups.     

Pain during injection of propofol: the effect of prior administration of butorphanol

Propofol causes pain or discomfort on injection in 28%-90% of patients. A number of techniques have been tried for minimizing propofol-induced pain with variable results. We compared the efficacy of butorphanol and lidocaine for prevention of propofol-induced pain. One-hundred-fifty ASA I-II adults, undergoing elective surgery were randomly assigned into 3 groups of 50 each. Group I (NS) received normal saline, Group II (L) received lidocaine 2% (40 mg), and Group III (B) received butorphanol 2 mg. All patients received pretreatment solutions made in 2 mL with normal saline administered over 5 s. One min after pretreatment patients received one-fourth of the total calculated dose of propofol (2.5 mg/kg) over 5 s. Assessment of pain with IV propofol was done by using a four-point scale: 0 = no pain, 1 = mild pain, 2 = moderate pain and 3 = severe pain at the time of propofol injection. In the control Group 39 (78%) patients had pain during propofol injection as compared to 21 (42%) and 10 (20%) in the lidocaine and butorphanol groups, respectively (P < 0.05). Butorphanol was the most effective. We therefore suggest the IV pretreatment with butorphanol 2 mg for attenuation of pain associated with propofol injection.     

Double-blind, Randomized Comparison of Ondansetron and Intraoperative Propofol to Prevent Postoperative Nausea And Vomiting

Background: Breast surgery is associated with a high incidence of postoperative nausea and vomiting. Propofol and prophylactic administration of ondansetron are associated with a lower incidence of postoperative nausea and vomiting. To date no comparison of these two drugs has been reported. A randomized study was done to compare the efficacy of ondansetron and intraoperative propofol given in various regimens.

Methods: Study participants included 89 women classified as American Society of Anesthesiologists physical status 1 or 2 who were scheduled for major breast surgery. Patients were randomly assigned to one of four groups. Group O received 4 mg ondansetron in 10 ml 0.9% saline and groups PI, PIP, and PP received 10 ml 0.9% saline before anesthesia induction. Group O received thiopental, isoflurane, nitrous oxide-oxygen, and fentanyl for anesthesia. Group PI received propofol, isoflurane, nitrous oxide-oxygen, and fentanyl. Group PIP received propofol, isoflurane, nitrous oxide-oxygen, and fentanyl. Thirty minutes before expected skin closure, isoflurane was discontinued and 50 to 150 micro gram [centered dot] kg sup -1 [centered dot] min sup -1 propofol was given intravenously to maintain anesthesia. Group PP received propofol for induction and maintenance of anesthesia, nitrous oxide-oxygen, and fentanyl. Postoperative pain relief was provided with morphine administered by a patient-controlled analgesia pump. The incidence of nausea and vomiting, requests for rescue antiemetic and sedation, pain scores, and hemodynamic data were recorded for 24 h.

Results: Within 6 h of surgery, groups O and PP had a lower incidence of nausea compared with groups PI and PIP (P < 0.05). Fewer patients in group PP (19%) vomited during the 24-h period compared with groups O (48%), PI (64%), and PIP (52%) (P < 0.05). The incidence of antiemetic use was also less in group PP (P < 0.05). Patients in group PP had lower sedation scores at 30 min and at 1 h (P < 0.05). There were no differences among the groups in pain scores, blood pressure, heart rate, respiratory rate, and incidence of pruritus.     

The effect of fentanyl on hemodynamic and bispectral index changes during anesthesia induction with propofol

STUDY OBJECT: To investigate the changes in hemodynamics and hypnotic levels during propofol infusion and tracheal intubation with and without fentanyl. DESIGN: Randomized, double-blinded study. SETTING: Teaching hospital. PATIENTS: 40 ASA physical status I adult patients scheduled for elective surgery. INTERVENTIONS: Patients were anesthetized with either propofol (Group P; n = 20) or 2 microg/kg of fentanyl IV followed by propofol (Group PF; n = 20). Propofol was infused at 20 mg/kg/hr throughout the study, and tracheal intubation was performed 10 minutes after the start of propofol infusion. MEASUREMENT AND MAIN RESULTS: Bispectral index monitoring (BIS) progressively decreased to about 50 in both groups during infusion of propofol, but no difference was found between the two groups. After tracheal intubation, BIS significantly increased but remained below 60 in both groups. Hypertensive responses to intubation were fewer in Group PF than Group P. CONCLUSIONS: Propofol administration 20 mg/kg/hr for 10 minutes is suitable in suppressing arousal reactions to tracheal intubation, but the addition of fentanyl is required to blunt the hemodynamic responses.     

A comparison between midazolam co-induction and propofol predosing for the induction of anaesthesia in the elderly

In a prospective, double-blind, randomised, placebo-controlled trial, we have compared the effects of midazolam co-induction with propofol predosing on the induction dose requirements of propofol in elderly patients. We enrolled 60 patients aged > 70 years, attending for urological surgery. The patients were allocated randomly to one of three groups, to receive either midazolam 0.02 mg.kg(-1), propofol 0.25 mg.kg(-1), or normal saline 2 ml (placebo) 2 min prior to induction of anaesthesia using propofol 1% infusion at 300 ml.h(-1). The propofol dose requirements for induction were recorded for two end-points (loss of verbal contact and insertion of an oropharyngeal airway). Cardiovascular parameters were recorded at 1-min intervals for each patient until induction was complete. The midazolam group showed a significant reduction in propofol dose requirements for induction (p = 0.05) compared to the placebo group. The propofol group did not show a significant dose reduction compared to placebo. There were no demonstrable differences in terms of improved cardiovascular stability between groups. We conclude that propofol predosing does not significantly reduce the induction dose of propofol required in the elderly, and there were no cardiovascular benefits to either midazolam co-induction or propofol predosing in the elderly.     

Effects of remifentanil and alfentanil on seizure duration, stimulus amplitudes and recovery parameters during ECT

BACKGROUND AND OBJECTIVE: Propofol may decrease seizure duration in electroconvulsive therapy. Although not proven, prolonged seizures may be more efficacious. The goal of this study was to evaluate and compare effects of alfentanil and remifentanil on seizure duration, recovery parameters and degree of stimulus amplitude in patients undergoing electroconvulsive therapy. METHODS: Twenty-four ASA I-II patients enrolled in this prospective, randomized trial, each receiving a total of seven electroconvulsive therapies. Patients were randomized to receive only Propofol, group P (0.75 mg kg-1, n=8), Propofol with alfentanil, group A (10 microg kg-1 alfentanil+0.5 mg kg-1 Propofol, n=8) and Propofol with remifentanil, group R (1 microg kg-1 remifentanil +0.5 mg kg-1 propofol, n=8) via an iv route. Supplemental doses of propofol were given as required to achieve loss of consciousness. Succinylcholine 0.5 mg kg-1 iv was given to all groups for muscular paralysis. We recorded hemodynamic parameters, cortical and motor seizure durations, and recovery parameters. RESULTS: Mean motor seizure duration was found to be significantly longer in patients receiving propofol-remifentanil anesthesia (53.3+/-13.6 s) and propofol-alfentanil anesthesia (52.2+/-0.4 s) compared with propofol anesthesia (37.6+/-9.2 s) (P=0.001). Recovery parameters and stimulus amplitudes were similar in groups A and R; significantly different from group P (P=0.001). CONCLUSIONS: Adding 10 microg kg-1 alfentanil or 1 microg kg-1 remifentanil to reduced doses of propofol provided unconsciousness and increased seizure durations. For patients who need higher stimulus amplitudes for longer seizure durations, combining low-dose propofol with alfentanil or remifentanil may be good alternative regimens for ECT.