Washout Of Sevoflurane Research Articles

Wash-in and wash-out of sevoflurane in a test-lung model: A comparison between Aisys and FLOW-i

Background:Modern anaesthesia workstations are reassuringly tight and are equipped with effective gas monitoring, thus providing good opportunities for low/minimal flow anaesthesia. A prerequisite for effective low flow anaesthesia is the possibility to rapidly increase and decrease gas concentrations in the circle system, thereby controlling the depth of anaesthesia. Methods:We studied the wash-in and wash-out of sevoflurane in the circle system with fixed fresh gas flow and vaporizer setting. We compared two modern anaesthesia work stations, the Aisys (GE, Madison, WI, USA) and FLOW-i (Maquet, Solna, Sweden) in a test lung model. Results: We found fresh-gas flow to have, as expected, a major influence on wash-in, as well as wash-out of sevoflurane. The wash-in time to reach a stable circle 1 MAC (2.1%) decreased from an average of 547 ± 83 seconds with a constant fresh gas flow of 300 ml/min and vaporizer setting of 8%, to a mean of 38 ± 6 seconds at a fresh gas flow of 4 L/min. There were only minor differences between the two works-stations tested; the Aisys was slightly faster at both 300 and 4 L/min flow. Time to further increase circle end-tidal concentration from 1-1.5 MAC showed likewise significant associations to fresh gas and decreased from 330 ± 24 seconds at 300 ml/min. to less than a minute at constant 4 L/min (17 ± 11 seconds), without anaesthetic machine difference. Wash-out was also fresh gas flow dependent and plateaued at 7.5 L/min. Conclusions: Circle system wash-in and wash-out show clear fresh gas dependency and varies somewhat between the Aisys and Flow-i. The circle saturation, reaching 1 MAC end-tidal or increasing from 1-1.5 MAC can be achieved with both work-stations within 1.5 minutes at a constant fresh gas flow of 2 and 4 L/min. Wash-out plateaued at 7.5 L/min.

Wash-in and wash-out of sevoflurane in a test-lung model: A comparison between Aisys and FLOW-i

Background: Modern anaesthesia workstations are reassuringly tight and are equipped with effective gas monitoring, thus providing good opportunities for low/minimal flow anaesthesia. A prerequisite for effective low flow anaesthesia is the possibility to rapidly increase and decrease gas concentrations in the circle system, thereby controlling the depth of anaesthesia. Methods: We studied the wash-in and wash-out of sevoflurane in the circle system with fixed fresh gas flow and vaporizer setting. We compared two modern anaesthesia work stations, the Aisys (GE, Madison, WI, USA) and FLOW-i (Maquet, Solna, Sweden) in a test lung model. Results: We found fresh-gas flow to have, as expected, a major influence on wash-in, as well as wash-out of sevoflurane. The wash-in time to reach a stable circle 1 MAC (2.1%) decreased from an average of 547 ± 83 seconds with a constant fresh gas flow of 300 ml/min and vaporizer setting of 8%, to a mean of 38 ± 6 seconds at a fresh gas flow of 4 L/min. There were only minor differences between the two works-stations tested; the Aisys was slightly faster at both 300 and 4 L/min flow. Time to further increase circle end-tidal concentration from 1-1.5 MAC showed likewise significant associations to fresh gas and decreased from 330 ± 24 seconds at 300 ml/min. to less than a minute at constant 4 L/min (17 ± 11 seconds), without anaesthetic machine difference. Wash-out was also fresh gas flow dependent and plateaued at 7.5 L/min. Conclusions: Circle system wash-in and wash-out show clear fresh gas dependency and varies somewhat between the Aisys and Flow-i. The circle saturation, reaching 1 MAC end-tidal or increasing from 1-1.5 MAC can be achieved with both work-stations within 1.5 minutes at a constant fresh gas flow of 2 and 4 L/min. Wash-out plateaued at 7.5 L/min.

Wash-in and wash-out of sevoflurane in a test-lung model: A comparison between Aisys and FLOW-i.

Background: Modern anaesthesia workstations are reassuringly tight and are equipped with effective gas monitoring, thus providing good opportunities for low/minimal flow anaesthesia. A prerequisite for effective low flow anaesthesia is the possibility to rapidly increase and decrease gas concentrations in the circle system, thereby controlling the depth of anaesthesia. Methods: We studied the wash-in and wash-out of sevoflurane in the circle system with fixed fresh gas flow and vaporizer setting. We compared two modern anaesthesia work stations, the Aisys (GE, Madison, WI, USA) and FLOW-i (Maquet, Solna, Sweden) in a test lung model. Results: We found fresh-gas flow to have, as expected, a major influence on wash-in, as well as wash-out of sevoflurane. The wash-in time to reach a stable circle 1 MAC (2.1%) decreased from an average of 547 ± 83 seconds with a constant fresh gas flow of 300 ml/min and vaporizer setting of 8%, to a mean of 38 ± 6 seconds at a fresh gas flow of 4 L/min. There were only minor differences between the two works-stations tested; the Aisys was slightly faster at both 300 and 4 L/min flow. Time to further increase circle end-tidal concentration from 1-1.5 MAC showed likewise significant associations to fresh gas and decreased from 330 ± 24 seconds at 300 ml/L to less than a minute at constant 4 L/min (17 ± 11 seconds), without anaesthetic machine difference. Wash-out was also fresh gas flow dependent and plateaued at 7.5 L/min. Conclusions: Circle system wash-in and wash-out show clear fresh gas dependency and varies somewhat between the Aisys and Flow-i. The circle saturation, reaching 1 MAC end-tidal or increasing from 1-1.5 MAC can be achieved with both work-stations within 1.5 minutes at a constant fresh gas flow of 2 and 4 L/min. Wash-out plateaued at 7.5 L/min.

Investigation of optical neuro-monitoring technique for detection of maintenance and emergence states during general anesthesia.

The American Society of Anesthesiologist recommends peripheral physiological monitoring during general anesthesia, which offers no information regarding the effects of anesthetics on the brain. Since no "gold standard" method exists for this evaluation, such a technique is needed to ensure patient comfort, procedure quality and safety. In this study we investigated functional near infrared spectroscopy (fNIRS) as possible monitor of anesthetic effects on the prefrontal cortex. Anesthetic drugs, such as sevoflurane, suppress the cerebral metabolism and alter the cerebral blood flow. We hypothesize that fNIRS derived features carry information on the effects of anesthetics on the prefrontal cortex (PFC) that can be used for the classification of the anesthetized state. In this study, patients were continuously monitored using fNIRS, BIS and standard monitoring during surgical procedures under sevoflurane general anesthesia. Maintenance and emergence states were identified and fNIRS features were identified and compared between states. Linear and non-linear machine learning algorithms were investigated as methods for the classification of maintenance/emergence. The results show that changes in oxygenated (HbO2) and deoxygenated hemoglobin (HHb) concentration and blood volume measured by fNIRS were associated with the transition between maintenance and emergence that occurs as a result of sevoflurane washout. We observed that during maintenance the signal is relatively more stable than during emergence. Maintenance and emergence states were classified with 94.7% accuracy with a non-linear model using the locally derived mean total hemoglobin, standard deviation of HbO2, minimum and range of HbO2 and HHb as features. These features were found to be correlated with the effects of sevoflurane and to carry information that allows real time and automatic classification of the anesthetized state with high accuracy.

Isocapnic hyperventilation shortens washout time for sevoflurane - an experimental in vivo study.

Isocapnic hyperventilation (IHV) is a method that fastens weaning from inhalation anaesthesia by increasing airway concentration of carbon dioxide (CO2 ) during hyperventilation (HV). In an animal model, we evaluated a technique of adding CO2 directly to the breathing circuit of a standard anaesthesia apparatus. Eight anaesthetised pigs weighing 28 ± 2 kg were intubated and mechanically ventilated. From a baseline ventilation of 5 l/min, HV was achieved by doubling minute volume and fresh gas flow. Respiratory rate was increased from 15 to 22/min. The CO2 absorber was disconnected and CO2 was delivered (DCO2 ) to the inspiratory limb of a standard breathing circuit via a mixing box. Time required to decrease end-tidal sevoflurane concentration from 2.7% to 0.2% was defined as washout time. Respiration and haemodynamics were monitored by blood gas analysis, spirometry, electric impedance tomography and pulse contour analysis. A DCO2 of 261 ± 19 ml/min was necessary to achieve isocapnia during HV. The corresponding FICO2 -level remained stable at 3.1 ± 0.3%. During IHV, washout of sevoflurane was three times faster, 433 ± 135 s vs. 1387 ± 204 s (P < 0.001). Arterial CO2 tension and end-tidal CO2 , was 5.2 ± 0.4 kPa and 5.6 ± 0.4%, respectively, before IHV and 5.1 ± 0.3 kPa and 5.7 ± 0.3%, respectively, during IHV. In this experimental in vivo model of isocapnic hyperventilation, the washout time of sevoflurane anaesthesia was one-third compared to normal ventilation. The method for isocapnic hyperventilation described can potentially be transferred to a clinical setting with the intention to decrease emergence time from inhalation anaesthesia.

Evaluation of Waste Anesthetic Gas in the Postanesthesia Care Unit within the Patient Breathing Zone.

Potential health hazards from waste anesthetic gases (WAGs) have been a concern since the introduction of inhalational anesthetics into clinical practice. The potential to exceed recommended exposure levels (RELs) in the postanesthesia care unit (PACU) exists. The aim of this pilot study was to assess sevoflurane WAG levels while accounting for factors that affect inhalational anesthetic elimination. In this pilot study, 20 adult day surgery patients were enrolled with anesthesia maintained with sevoflurane. Following extubation, exhaled WAG from the patient breathing zone was measured 8 inches from the patient's mouth in the PACU. Maximum sevoflurane WAG levels in the patient breathing zone exceeded National Institute for Occupational Safety and Health (NIOSH) RELs for every 5-minute time interval measured during PACU Phase I. Observed WAGs in our study were explained by inhalational anesthetic pharmacokinetics. Further analysis suggests that the rate of washout of sevoflurane was dependent on the duration of anesthetic exposure. This study demonstrated that clinically relevant inhalational anesthetic concentrations result in sevoflurane WAG levels that exceed current RELs. Evaluating peak and cumulative sevoflurane WAG levels in the breathing zone of PACU Phase I and Phase II providers is warranted to quantify the extent and duration of exposure.

Effects of fresh gas flow, tidal volume, and charcoal filters on the washout of sevoflurane from the Datex Ohmeda (GE) Aisys, Aestiva/5, and Excel 210 SE Anesthesia Workstations.

We investigated the effects of tidal volume (VT), fresh gas flow (FGF), and a charcoal filter in the inspiratory limb on the washout of sevoflurane from the following Datex Ohmeda (GE) Anesthesia Workstations (AWSs): Aisys, Aestiva/5, and Excel 210SE. After equilibrating the AWSs with 2% sevoflurane, the anesthetic was discontinued, and the absorbent anesthesia breathing circuit (ABC), reservoir bag, and test lung were changed. The lung was ventilated with 350 or 200 mL·breath(-1), 15 breaths·min(-1), and a FGF of 10 L·min(-1) while the washout of sevoflurane was performed in triplicate using a calibrated Datex Ohmeda Capnomac Ultima™ and a calibrated MIRAN SapphIRe XL ambient air analyzer until the concentration was ≤ 10 parts per million (ppm). The effects of decreasing the FGF to 5 and 2 L·min(-1) after the initial washout and of a charcoal filter in the ABC were recorded separately. The median washout times with the Aisys AWS (14 min, P < 0.01) and the Aestiva/5 (17 min, P < 0.001) with VT 350 mL·breath(-1) were significantly less than that with the Excel 210SE (32 min). The mean (95% confidence interval) washout time with the Aisys increased to 23.5 (21.5 to 25.5) min with VT 200 mL·breath(-1) (P < 0.01). Decreasing the FGF from 10 to 5 and 2 L·min(-1) with the Aisys caused a rebound in sevoflurane concentration to ≥ 50 ppm. Placement of a charcoal filter in the inspiratory limb reduced the sevoflurane concentration to < 2 ppm in the Aisys and Aestiva/5 AWSs within two minutes. The GE AWSs should be purged with large FGFs and VTs ~350 mL·breath(-1) for ~25 min to achieve 10 ppm sevoflurane. The FGF should be maintained to avoid a rebound in anesthetic concentration. Charcoal filters rapidly decrease the anesthetic concentration to < 2 ppm.

The sevoflurane washout profile of seven recent anesthesia workstations for malignant hyperthermia-susceptible adults and infants: a bench test study.

Preoperative flushing of an anesthesia workstation is an alternative for preparation of the anesthesia workstation before use in malignant hyperthermia-susceptible patients (MHS). We studied in vitro, using a test lung, the washout profile of sevoflurane in 7 recent workstations during adult and, for the first time, pediatric ventilation patterns. Anesthesia workstations were first primed with 3% sevoflurane for 2 hours and then prepared according to the recommendations of the Malignant Hyperthermia Association of the United States. The flush was done with maximal fresh gas flow (FGF) with a minute ventilation equal to 600 mL × 15, to reach a sevoflurane concentration of <5 parts per million. After flush, 2 clinical situations were simulated in vitro to test the efficiency of preparation: decrease of FGF from max to 10 L/min, or decrease of minute ventilation to 50 mL × 30, to simulate the ventilation of an MHS infant. We report washout delays for MHS patients for previously studied workstations (Primus®, Avance®, and Zeus®) and more interestingly, for machines not previously tested (Felix®, Flow-I®, Perseus®, and Leon®). An increase of sevoflurane concentration was observed when decreasing FGF (except for flow-I® and Leon®) and during simulation of MHS infant ventilation (except for Felix®). This descriptive study strongly suggests that washout profiles may differ for each anesthesia workstation. We advise the use of maximal FGF during preparation and anesthesia. Required flushing times are longer when preparing an anesthesia workstation before providing anesthesia for MHS infants.

Pharmacokinetics of sevoflurane elimination from respiratory gas and blood after coronary artery bypass grafting surgery.

Sevoflurane, with a relative low blood-gas partition coefficient, is an ideal anesthetic to achieve rapid offset and recovery from general anesthesia. This study will determine the profiles of four concentration-time curves to characterize the pharmacokinetics of sevoflurane elimination. Eight patients (aged 54-76 years) undergoing coronary arterial bypass grafting surgery were enrolled in this study. At the end of surgery, anesthetic gas and blood were sampled 20 min before and after stopping sevoflurane administration, with prior maintenance of a fixed 5% inspired sevoflurane (CIsev) in 6 L/min oxygen flow for 60 min before the cessation of sevoflurane administration for the subsequent 20 min elimination. An infrared analyzer was used to determine both CIsev and end-tidal sevoflurane (CEsev). The sevoflurane concentrations in the internal jugular-bulb (Jsev), arterial (Asev) and pulmonary arterial blood (PAsev) were analyzed by gas chromatography, and cardiac output was measured using an Opti-Q pulmonary artery catheter. A bi-exponential decay function was the best fit for the CEsev,Jsev, Asev, and PAsev time curves. There were two distinct components, the initial 5-min fast or distribution phase and the subsequent 15-min slow or elimination phase. Before cessation of the sevoflurane supplement, the step-down concentration of sevoflurane was listed in the following order: CIsev > CEsev > Asev ≧ Jsev > PAsev. During the elimination phase, the fastest decay occurred in CEsev, followed by Jsev, Asev and PAsev. Therefore, a reverse step-down pattern was observed (PAsev > Asev ≧ Jsev > CEsev) after 20 min. The ratio of Asev to CEsev was 89% at baseline before stopping sevoflurane administration, but the ratio of Asev to CEsev increased to 128% at the twentieth min of the sevoflurane elimination phase. During elimination, the initial washout of sevoflurane from the functional residual capacity of the lungs was reflected in the fast component of the CEsev, Jsev, Asev, and PAsev time curves. In contrast, the slow component was dominated by the tangible effects of the physiological membrane barriers, such as the alveoli-pulmonary capillary and blood-brain barriers.

Age-related changes in EEG power spectra in infants during sevoflurane wash-out

Few electroencephalography (EEG) data are available in anaesthetized infants. This study aimed to identify EEG characteristics that might warn of awakening (AW) from sevoflurane anaesthesia in infants. Twenty intubated infants [aged 39-77 weeks post-menstrual age (PMA)] were studied after surgery during sevoflurane wash-out. EEG was recorded at the end of surgery and throughout emergence. Changes in EEG time and frequency domains were described. At the end of surgery, mean end-tidal sevoflurane concentration was 2.3% (range 1.5-3.5) before wash-out and reduced to 0.3% (0.1-0.6) when AW began. On AW, movement artifacts made signals difficult to interpret. Before awakening, most power was within frequencies ≤4 Hz, but trends over time were variable. Summated power in frequencies between 20 and 70 Hz was almost always <5 µV(2). During anaesthesia, there were two common power spectra: infants >52 weeks PMA had obvious summated power in the frequency range 5-20 Hz (P5-20 Hz) (mean 308, median 320, range 110-542 µV(2)), which decreased before awakening began [mean decrease 252 µV(2) (95% CI 153-351)], whereas younger infants had low P5-20 Hz throughout. P5-20 Hz during anaesthesia increased with age; power in this frequency band of ~100 µV(2) separated infants younger and older than 52 weeks PMA. During sevoflurane wash-out, decreasing P5-20 Hz might warn of impending AW in infants >3 months old, but not in younger infants.

Comparison of emergence agitation between sevoflurane/nitrous oxide administration and sevoflurane administration alone in children undergoing adenotonsillectomy with preemptive ketorolac

BackgroundSevoflurane anesthesia commonly causes emergence agitation (EA) in children. One previous study has reported that the use of nitrous oxide (N2O) during the washout of sevoflurane may reduce EA by decreasing the residual sevoflurane concentration, while many animal studies suggest that N2O poses a potential risk to children. The present study was designed to compare EA in children assigned to receive sevoflurane with N2O (group N) or sevoflurane alone (group S).MethodsWe enrolled 80 children aged 3-10 years. Anesthesia was induced with 5 mg/kg thiopental sodium, 0.6 mg/kg rocuronium and 0.5 mg/kg ketorolac, and was maintained with 50% N2O and sevoflurane in group N or with sevoflurane alone in group S. The sevoflurane concentration was adjusted with a bispectral index (BIS) of 40-60. After completion of the surgery, N2O and sevoflurane were simultaneously discontinued and replaced with oxygen (O2) at 6 L/min. End-tidal sevoflurane concentration (Et Sevo) (%), BIS at the end of surgery, Et Sevo at recovery of self-respiration and emergence profiles were recorded. EA occurrence, pain score and rescue fentanyl consumption were assessed in the postanesthesia care unit.ResultsEt Sevo was significantly lower in group N (1.9%) than in group S (2.3%) at the end of surgery. However, there were no differences in Et Sevo at recovery of self-respiration, emergence times, the incidence of EA, pain score or dose of rescue fentanyl between the groups.ConclusionsIn children undergoing adenotonsillectomy with preemptive ketorolac, anesthetic maintenance using sevoflurane alone does not affect the incidence of EA or emergence profiles compared to anesthetic maintenance using sevoflurane with N2O.

Metabotropic actions of the volatile anaesthetic sevoflurane increase protein kinase Mζ synthesis and induce immediate preconditioning protection of rat hippocampal slices

Anaesthetic preconditioning occurs when a volatile anaesthetic, such as sevoflurane, is administered before a hypoxic or ischaemic insult; this has been shown to improve neuronal recovery after the insult. We found that sevoflurane-induced preconditioning in the rat hippocampal slice enhances the hypoxic hyperpolarization of CA1 pyramidal neurons, delays and attenuates their hypoxic depolarization, and increases the number of neurons that recover their resting and action potentials after hypoxia. These altered electrophysiological effects and the improved recovery corresponded with an increase in the amount of a constitutively active, atypical protein kinase C isoform found in brain, protein kinase M zeta (PKMζ). A selective inhibitor of this kinase, zeta inhibitory peptide (ZIP), blocked the increase in the total amount of PKMζ protein and the amount of the activated form of this kinase, phospho-PKMζ (p-PKMζ); it also blocked the altered electrophysiological effects and the improved recovery. We found that both cycloheximide, a general protein synthesis inhibitor, and rapamycin, a selective inhibitor of the mTOR pathway for regulating protein synthesis, blocked the increase in p-PKMζ, the electrophysiological changes, and the improved recovery due to sevoflurane-induced preconditioning. Glibenclamide, a KATP channel blocker, when present only during the hypoxia, prevented the enhanced hyperpolarization, the delayed and attenuated hypoxic depolarization, and the improved recovery following sevoflurane-induced preconditioning. To examine the function of persistent PKMζ and KATP channel activity after the preconditioning was established, we administered 4% sevoflurane for 30 min and then discontinued it for 30 min before 10 min of hypoxia. When either tolbutamide, a KATP channel blocker, or ZIP were administered at least 15 min after the washout of sevoflurane, there was little recovery compared with sevoflurane alone. Thus, continuous KATP channel and PKMζ activity are required to maintain preconditioning protection. We conclude that sevoflurane induces activation of the mTOR pathway, increasing the new protein synthesis of PKMζ, which is constitutively phosphorylated to its active form, leading to an increased KATP channel-induced hyperpolarizaton. This hyperpolarization delays and attenuates the hypoxic depolarization, improving the recovery of neurons following hypoxia. Thus, sevoflurane acts via a metabotropic pathway to improve recovery following hypoxia.

Washout of sevoflurane from the GEAvance and Amingo Carestation anesthetic machines

Inhalational anesthetics must be removed from anesthetic machines to prevent malignant hyperthermia (MH) in susceptible patients or to treat MH occurring during inhalational general anesthesia. This study examines the sevoflurane washout from the GE Avance and Amingo Carestations™. The care stations were contaminated with sevoflurane during general anesthesia. Then, the vaporizer was removed, the CO₂ absorber was exchanged against an empty one and the breathing tubes were substituted by clean ones. In the first part, the fresh gas flow was 10 l/min. In the second part, the Advanced Breathing System™ (ABS™), the internal breathing circuit, was replaced by a laundered component. The fresh gas flow was set to 10 l/min for 10 min and to 5 l/min for the following 20 min. In the 25 measurements of the first part, the sevoflurane concentration decreased from a median of 31.60 ppm [interquartile range (IQR) 130.12 ppm] within 22 min in every case to values below 5 ppm and stayed there for the last 8 min of the measuring (P < 0.0001). In the 15 measurements of the second part, the sevoflurane concentration fell from the median of 8.56 ppm (IQR 8.99 ppm) within 5 min to values being significantly below 5 ppm and stayed there for the following 25 min (P < 0.0001). In case of sudden onset of MH, the Avance or Amingo Carestation™ can stay in place, if the fresh gas flow is increased to 10 l/min or more. To prepare these machines for MH-susceptible patients, the ABS™ should be substituted by a laundered component.

The influence of sevoflurane on the bispectral index, regional cerebral oxygen saturation, and propofol concentration during propofol/N2O anesthesia

This study was undertaken to investigate the influence of sevoflurane on the bispectral index (BIS), regional cerebral oxygen saturation (rSO(2)), and serum propofol concentration during propofol/N(2)O anesthesia. This study tested the hypothesis that sevoflurane affect BIS values, rSO(2), and the pharmacokinetics of propofol during propofol/ N(2)O anesthesia. General anesthesia was administered to 15 ASA I-II patients with a continuous infusion of propofol to maintain a BIS value of 45 +/- 5. After recording baseline values, patients were assigned to receive sevoflurane (2.0%, 20 min). BIS values, rSO(2) using near-infrared spectroscopy, and hemodynamic parameters were recorded for 60 min. Cardiac output (CO) and stroke volume (SV) were evaluated using impedance cardiograph methods. Propofol concentration was determined using high-performance liquid chromatography. Sevoflurane (2.0%, 20 min) decreased the BIS score from 47.4 +/- 8.2 to 27.3 +/- 5.9 (P < 0.01, n = 15) without affecting rSO(2). Sevoflurane decreased systolic blood pressure from 112.1 +/- 14.0 mmHg to 96.5 +/- 13.2 mmHg (P < 0.001, n = 15) without affecting heart rate. Both CO and SV were significantly decreased during sevoflurane application. Propofol concentration was increased from 2.71 +/- 0.51 microg/ml to 3.30 +/- 0.57 microg/ml (P < 0.05) after sevoflurane application, and was returned to baseline after sevoflurane washout. We have shown that sevoflurane decreases BIS values during propofol/N(2)O anesthesia without affecting rSO(2) and that this change is accompanied by an increase in serum propofol concentration. Changes in propofol concentration may be due to, at least in part, hemodynamic changes such as decreased CO produced by sevoflurane.

Nitrous oxide administration during washout of sevoflurane improves postanesthetic agitation in children

The use of sevoflurane in pediatric patients, which could enable a more rapid emergence and recovery, is complicated by a high incidence of postanesthetic agitation, probably due to residual sevoflurane during washout. The present study was designed to investigate whether administration of nitrous oxide (N2O) reduces sevoflurane concentration at awakening and suppresses postanesthetic agitation. The study enrolled 20 children classified as ASA physical status I. Anesthesia was induced with 5% sevoflurane and maintained with 2.5% end-tidal sevoflurane and N2O in oxygen. In the control group, sevoflurane and N2O were discontinued immediately after completion of surgery. In the N2O group, inspired N2O was replaced with oxygen after the bispectral index (BIS) had reached 80. The end-tidal concentrations of sevoflurane at awakening were significantly lower (P < 0.05) in the N2O group than in the control group. The BIS at awakening was higher (P < 0.01) in the N2O group than in the control group. The point scores of postanesthetic agitation were significantly lower (P < 0.01) in the N2O group than in the control group. Using N2O during washing out of sevoflurane may improve postanesthetic agitation at awakening in children.

The Effect of Fresh Gas Flow on Sevoflurane Concentrations during Emergence from Anesthesia

Background: Fresh gas flow (FGF) influences the speeds of induction and emergence. In general, emergence protocol involves a stepwise decrease in the vaporizer setting at fixed FGF, which causes anesthetic overuse and contaminates operating rooms. This study was designed to compare the decreasing patterns of sevoflurane concentration among groups with a similar course but with different FGFs. Methods: One hundred patients scheduled for elective operation were randomly allocated to 3 groups (FGF 1 L/min, FGF 2 L/min, FGF 4 L/min). After induction with thiopental sodium 5 mg/kg and rocuronium 0.9 mg/kg or vecuronium 0.1 mg/kg for tracheal intubation, anesthesia was maintained at 1.5% of end-tidal sevoflurane concentration at an inflow of 4 L/min ( 2 L/min and 2 L/min). Ten minutes prior to the estimated operation end point, we changed FGF and vaporizer settings to the following 3 different emergence protocols: changing inflow in the FGF 1 L/min group ( 0.5 L/min and 0.5 L/min) with turning vaporizer off, changing inflow in the FGF 2 L/min group ( 1 L/min and 1 L/min) with a two-step decrease in the vaporizer setting (1.0 vol% for first 5 minutes then with the vaporizer off), and maintaining the inflow in the FGF 4 L/min group with a three-step decrease in the vaporizer setting (1.0 vol% for first 5 minutes and 0.6 vol% for next 5 minutes then with the vaporizer off). In each group, inspiratory and end-tidal sevoflurane concentrations were recorded every minute for 16 minutes, while end-tidal , mean arterial pressure, heart rate, and inspired oxygen fraction were recorded every two minutes for 16 minutes. Results: End-tidal concentrations of sevoflurane were similar in the 3 groups at the 6th, and 7th minutes and continuously increasing differences in sevoflurane concentrations from the 11th to 16th minute were observed in the FGF 1 L/min and FGF 2 L/min groups versus the FGF 4 L/min group. The concentration curves for the FGF 1 L/min group showed a smoother decreasing pattern than those of the other groups. Conclusions: The use of low FGF without vaporizer during emergence reduces sevoflurane washout within anesthetic machines and the exhausting of anesthetics into operating rooms, and also offers an easier means of controlling anesthetic depth.

The action of sevoflurane on vascular smooth muscle of isolated mesenteric resistance arteries (part 1): role of endothelium.

The direct action of sevoflurane on systemic resistance arteries is not fully understood. Isometric force was recorded in isolated rat small mesenteric arteries. Sevoflurane (2-5%) enhanced contractile response to norepinephrine only in the presence of endothelium, but inhibited it in its absence. Sevoflurane still enhanced the norepinephrine response after inhibitions of the nitric oxide, endothelium-derived hyperpolarizing factor, cyclooxygenase and lipoxygenase pathways, or after blockade of either endothelin-1 ET-1), angiotensin-II, or sevotonin receptors. Sevoflurane (3-5%) inhibited contractile response to potassium chloride only in the absence of endothelium but did not influence it in its presence. In the endothelium-intact strips, inhibition of the norepinephrine response, which was enhanced during application of sevoflurane, was observed after washout of sevoflurane and persisted for approximately 15 min. In the endothelium-denuded strips, the inhibition of norepinephrine response was similarly prolonged after washout of sevoflurane. However, no significant inhibitions of potassium chloride response were observed after washout of sevoflurane in both the endothelium-intact and the endothelium-denuded strips. The action of sevoflurane on norepinephrine contractile response consists of endothelium-dependent vasoconstricting and endothelium-independent vasodilating components. In the presence of endothelium, the former predominates over the latter, enhancing the norepinephrine response. The endothelium-independent component persisted after washout of sevoflurane, leading to prolonged inhibition of the norepinephrine response. The mechanisms behind the sevoflurane-induced inhibition of norepinephrine response are at least in part different from those behind its inhibition of potassium chloride response. Nitric oxide, endothelium-derived hyperpolarizing factor, cyclooxygenase products, lipoxygenase products, endothelin-1, angiotensin-II, and serotonin are not involved in the vasoconstricting action. (Key words: Halogenated volatile anesthetics; sympathetic nervous system; systemic hypotension; vascular endothelium.)