Effects of sevoflurane and isoflurane on systemic vascular resistance: use of cardiopulmonary bypass as a study model

We have examined the dose-related effects of sevoflurane and isoflurane on systemic vascular resistance (SVR) during cardiopulmonary bypass (CPB) in patients undergoing elective coronary artery surgery. Fifty- two patients were allocated randomly to one of six groups to receive 1.0, 2.0 or 3.0 vol% (inspiratory) sevoflurane or 0.6, 1.2 or 1.8 vol% isoflurane, or to a control group. During hypothermic (32-33 degrees C) non-pulsatile CPB, systemic vascular resistance index (SVRI) was recorded before administration of volatile anaesthetics and every 5 min for 20 min. Sevoflurane and isoflurane concentrations were measured next to the gas inlet port and at the gas outlet port of the oxygenator. Wash-in of sevoflurane occurred more rapidly than that of isoflurane, reaching a relatively steady state for both agents from the 10th to the 20th min. There was no significant change in SVRI in patients receiving 1.0 and 2.0 vol% sevoflurane, and 0.6 and 1.2 vol% isoflurane, compared with baseline values. However, 3 vol% sevoflurane decreased SVRI at 10, 15 and 20 min, and 1.8 vol% isoflurane decreased SVRI significantly at 15 and 20 min, whereas SVRI increased at 15 and 20 min in the control group. Thus during CPB, sevoflurane had similar vasodilator effects on SVRI as isoflurane.      

The in-vitro effects of sevoflurane and desflurane on the contractility of pregnant human uterine muscle

The effect of desflurane and sevoflurane on the contractility of the uterus was examined in vitro on strips of human myometrium obtained at the time of elective cesarean section. Small strips (1 mm x 2 mm x 10 mm) of muscle were prepared and suspended in an organ bath containing oxygenated physiological saline. Force of contraction was recorded continuously using an isometric tension transducer. Following the onset of regular spontaneous contractions, baseline measurements were obtained and the strips were exposed to varying concentrations of sevoflurane or desflurane corresponding to 0.5, 1.0 and 1.5 minimum alveolar concentration (MAC). Sevoflurane depressed contractility to 72 +/- 18% of control at 0.5 MAC, 37 +/- 15% at 1.0 MAC and 27 +/- 16% at 1.5 MAC compared with 65 +/- 14 of control at 0.5 MAC, 43 +/- 18% at 1.0 MAC and 22 +/- 11% at 1.5 MAC for desflurane. The degree of depression of uterine muscle contractility produced by both these agents was significantly different from control at all concentrations. In conclusion, both sevoflurane and desflurane depress the contractility of isolated pregnant human myometrium at concentrations of 0.5, 1.0 and 1.5 MAC. These agents produce a similar degree of depression of uterine muscle contractility.     

地氟醚、异氟醚和七氟醚对脑血流速率的影响

目的　通过经颅多普勒超声 (TCD)监测大脑中动脉 (MCA)血流速率 ,观察地氟醚、异氟醚和七氟醚三种吸入麻醉药对平均血流速率 (Vm)的影响。方法　 42例 18～ 6 0岁、ASAⅠ～Ⅱ级、择期非颅脑手术病人 ,随机接受地氟醚、异氟醚或七氟醚吸入麻醉。机械通气维持PETCO2 在 40± 1mmHg。当呼气末吸入麻醉药浓度分别为 :1 0MAC平衡 15分钟后 ,快速 (2分钟内 )从 1 0MAC升高至 1 5MAC即时 ,1 5MAC平衡 15分钟后 ,以及稳定于 1 5MAC并且维持和 1 0MAC平衡下相似的MAP时 ,记录Vm、MAP和心率。结果　 (1)吸入浓度从 1 0MAC上升至 1 5MAC ,且MAP维持相同水平的情况下 ,地氟醚和异氟醚使Vm增加非常显著 (分别从 5 6cm/s上升至 6 1cm/s,从47cm/s上升至 5 2cm/s,P <0 0 1) ,而七氟醚无显著变化 (从 6 0cm/s至 6 0cm/s,P >0 0 5 )。 (2 )当吸入浓度快速从 1 0MAC上升至 1 5MAC时 ,地氟醚使血压升高、心率增快 ,同时 ,脑血流速率显著增加 (从 5 6cm/s上升至 6 1cm/s,P <0 0 1)。而异氟醚和七氟醚在MAP显著下降的同时使Vm无显著变化 (从 47cm/s升至 49cm/s,P >0 0 5 ) ,或显著下降 (从 6 0cm/s降至 5 6cm/s,P <0 0 1)。结论　 (1)吸入浓度从 1 0MAC增加到 1 5MCA时 ,地氟醚、异氟醚使脑血流速率显著增加 ,而七氟醚作     

The effect of desflurane and sevoflurane on cerebral oximetry under steady-state conditions

We studied the effect of sevoflurane and desflurane on regional cerebral oxygenation (rSO2). Twenty-two patients undergoing abdominal hysterectomy received sevoflurane and desflurane for 15 min each and 30 min apart under steady-state conditions in a randomized, crossover manner to maintain a bispectral index (BIS) of 40-50. In another 22 patients undergoing the same anesthesia and surgery BIS was maintained at 20-30. During the 15-min administration of each anesthetic at steady-state conditions rSO2, BIS, inspired and end-tidal anesthetic concentrations, end-tidal CO2, Spo2, systolic and diastolic blood pressures, and heart rate were recorded every 3 min. The rSO2 did not differ between sevoflurane and desflurane when BIS values were maintained between 40-50 or 20-30. The MAC(BIS) values required to maintain BIS at 40-50 and at 20-30 were 1.0 versus 1.2 (P = 0.004) and 1.6 versus 1.8 (P < 0.001) for desflurane and sevoflurane respectively. Higher rSO2 values were obtained by 1.6 MAC (71 +/- 13) than by 1 MAC of desflurane (66 +/- 10; P < 0.001) and by 1.8 MAC (72 +/- 11) than by 1.2 MAC of sevoflurane (66 +/- 13; P < 0.001). In conclusion, equipotent concentrations of desflurane or sevoflurane in terms of BIS are associated with similar rSO2 values, but larger anesthetic concentrations of both anesthetics increased the rSO2 values.     

七氟醚、异氟醚和地氟醚对神经外科手术患者经颅电刺激运动诱发电位的影响

目的 比较七氟醚、异氟醚和地氟醚对神经外科手术患者经颅电刺激运动诱发电位(MEPs)的影响.方法 择期行神经外科手术患者60例,年龄18～64岁,ASA分级Ⅰ或Ⅱ级.随机分为3组(n=20):七氟醚组、异氟醚组和地氟醚组.监测BIS值和经颅电刺激MEPs.调节七氟醚、异氟醚和地氟醚吸入浓度,使其呼气末浓度分别达到0.50、0.75、1.00和1.30 MAC,每一浓度均维持15 min,视为稳态呼气末浓度.于给予吸入麻醉药前(基础状态)和达到各稳态呼气末浓度(T1-4)时,记录MEPs的波幅和潜伏期以及BIS值.记录MEPs波形记录失败情况.结果 与七氟醚组和异氟醚组比较,地氟醚组T1.2时波幅和BIS值降低,T1-4时潜伏期延长(P＜0.05);七氟醚组和异氟醚组各指标比较差异无统计学意义(P＞0.05).七氟醚组、异氟醚和地氟醚组基础状态、T1、T2时的记录失败率均为0;T3时记录失败率分别为0、5%和20%,三组比较差异无统计学意义(P＞0.05);T4时记录失败率分别为5%、20%和45%,与七氟醚组和异氟醚组比较,地氟醚组记录失败率升高(P＜0.05);七氟醚组和异氟醚组比较差异无统计学意义(P＞0.05).结论 地氟醚对神经外科手术患者经颅电刺激MEPs的抑制作用强于七氟醚和异氟醚.术中行MEPs监测时,七氟醚和异氟醚适宜的呼气末浓度为1.00 MAC,地氟醚为0.75～1.00 MAC.     

地氟烷和七氟烷在稳态条件下对脑氧饱和度的影响

我们研究了七氟烷和地氟烷对局部脑组织氧饱和度（rSO2）的影响。22例经腹行子宫切除术的患者在稳态条件下以随机交叉的方式间隔30分钟吸入七氟烷和地氟烷各15分钟，维持脑电双频指数（bispectral index，BIS）值为40～50。另一组接受同样手术和麻醉的22例患者维持BIS值为20—30。在每种麻醉药15分钟的维持期间，每3分钟记录一次稳态条件下的rSO2、BIS、麻醉药吸入浓度和呼气末浓度、呼气末二氧化碳、SpO2、舒张压和收缩压以及心率。当BIS值维持于40～50或20—30时，两种麻醉药的rSO2均无差异。维持BIS值为40～50和20—30所需地氟烷和七氟烷的MACBIS值分别为1．0和1．2（P=0．004）及1．6和1．8（P〈0．001）。吸入1．6MAC地氟烷的rSO，值（71±13）高于1MAC时的rSO2值（66±10，P〈0．001），吸入1．8MAC七氟烷的rSO2值（72±11）高于1．2MAC时的rSO2值（66±13，P〈0．001）。因此，BIS值等效浓度的地氟烷或七氟烷的rSO，值相似，而提高两种麻醉药的吸入浓度均可增加rSO2值。     

In vitro effects of desflurane, sevoflurane, isoflurane, and halothane in isolated human right atria

BACKGROUND: Direct myocardial effects of volatile anesthetics have been studied in various animal species in vitro. This study evaluated the effects of equianesthetic concentrations of desflurane, sevoflurane, isoflurane, and halothane on contractile parameters of isolated human atria in vitro. METHODS: Human right atrial trabeculae, obtained from patients undergoing coronary bypass surgery, were studied in an oxygenated (95% O2-5% CO2) Tyrode's modified solution ([Ca2+]o = 2.0 mM, 30 degrees C, stimulation frequency 0.5 Hz). The effects of equianesthetic concentrations (0.5, 1, 1.5, 2, and 2.5 minimum alveolar concentration [MAC]) of desflurane, sevoflurane, isoflurane, and halothane on inotropic and lusitropic parameters of isometric twitches were measured. RESULTS: Isoflurane, sevoflurane, and desflurane induced a moderate concentration-dependent decrease in active isometric force, which was significantly lower than that induced by halothane. In the presence of adrenoceptor blockade, the desflurane-induced decrease in peak of the positive force derivative and time to peak force became comparable to those induced by isoflurane. Halothane induced a concentration-dependent decrease in time to half-relaxation and a contraction-relaxation coupling parameter significantly greater than those induced by isoflurane, sevoflurane and desflurane. CONCLUSIONS: In isolated human atrial myocardium, desflurane, sevoflurane, and isoflurane induced a moderate concentration-dependent negative inotropic effect. The effect of desflurane on time to peak force and peak of the positive force derivative could be related to intramyocardial catecholamine release. At clinically relevant concentrations, desflurane, sevoflurane, and isoflurane did not modify isometric relaxation.     

The direct depressant effects of desflurane and sevoflurane on spontaneous contractions of isolated gravid rat myometrium

Our purpose was to investigate the direct depressant effects of desflurane and sevoflurane at 0.5, 1 and 2 minimum alveolar concentrations (MAC) on spontaneous contractions of isolated gravid rat myometrium. Ten gravid, albino Wistar rats, weighing 240-310 g and at 19-20 days' gestation were used. Sixty myometrial strips were obtained from 10 rats, and randomly assigned into six groups of 10. After obtaining spontaneous myometrial contractions in de Jalon solution for 45 min, 0.5, 1 or 2 MAC of desflurane or sevoflurane were continuously bubbled in the bath for 15 min and myometrial contractions evaluated during the last 10 min. Desflurane 0.5 MAC did not affect duration or amplitude of spontaneous contractions, but frequency was significantly decreased (P < 0.05). Duration, amplitude and frequency were all significantly decreased by desflurane 1 and 2 MAC (P < 0.05). Sevoflurane did not affect duration, amplitude or frequency at 0.5 MAC, but amplitude and frequency were significantly decreased at 1 MAC and all were significantly decreased at 2 MAC (P < 0.05). The frequency of contractions was decreased 21.2% with 1 MAC desflurane versus 17.1% with 1 MAC sevoflurane. The amplitude and frequency of contractions were decreased 48.2% and 48.7% with 2 MAC desflurane versus 58.9% and 49.3% with 2 MAC sevoflurane, respectively. We suggest that due to tocolytic activity, desflurane and sevoflurane can be useful in non-obstetric surgery during pregnancy.     

Effect of halothane, isoflurane and desflurane on lower oesophageal sphincter tone

We have studied the effects of volatile anaesthetics on lower oesophageal sphincter (LOS) tone in three groups of eight pigs allocated randomly to receive end-tidal concentrations of 0.5, 1.0 and 1.5 MAC of desflurane, isoflurane or halothane for 15 min. LOS and oesophageal barrier pressures (BrP = LOSP - gastric pressure) were measured using a manometric method. The decrease in BrP paralleled the decrease in LOS pressure and was significant at 0.5 MAC for isoflurane and at 1.0 MAC for halothane. At 1.5 MAC, BrP values were approximately 62% of baseline values for halothane, 37% for isoflurane and 83% for desflurane. Inter-group comparisons showed that BrP did not differ at baseline and at 0.5 MAC. At 1.0 MAC the effect of isoflurane on BrP was significantly different from desflurane (P < 0.001) and halothane (P < 0.02) whereas the effect of desflurane on BrP was not significantly different from halothane. At 1.5 MAC the effect of isoflurane on BrP was significantly different from desflurane (P < 0.01) and halothane (P < 0.05) whereas the effect of desflurane on BrP was not significantly different from halothane. We conclude that desflurane maintained BrP and this may be clinically important in patients at high risk of regurgitation.      

Beneficial effects of sevoflurane and desflurane against myocardial reperfusion injury after cardioplegic arrest

PURPOSE: To determine whether sevoflurane or desflurane offer additional protective effects against myocardial reperfusion injury after protecting the heart against the ischemic injury by cardioplegic arrest. METHODS: Isolated rat hearts in a Langendorff-preparation (n = 9) were arrested by infusion of HTK cardioplegic solution and subjected to 30 min global ischemia followed by 60 min reperfusion (controls). An additional 18 hearts were subjected to the same protocol, and sevoflurane (n = 9) or desflurane (n = 9) was added to the perfusion medium during the first 30 min of reperfusion in a concentration corresponding to 1.5 MAC in rats. Left ventricular (LV) developed pressure and creatine kinase (CK) release were determined as indices of myocardial performance and cellular injury, respectively. RESULTS: The LV developed pressure recovered to 46+/-7% of baseline in controls. Functional recovery during reperfusion was improved by inhalational anesthetics to 67+/-3% (sevoflurane, P<0.05) and 61+/-5% of baseline (desflurane, P<0.05), respectively. Peak CK release during early reperfusion was reduced from 52+/-11 U x min(-1) x g(-1) in controls to 34+/-7 and 26+/-7 U x min(-1) x g(-1) in sevoflurane and desflurane treated hearts, respectively. The CK release during the first 30 min of reperfusion was reduced from 312+/-41 U x g(-1) in control hearts to 195+/-40 and 206+/-37 U x g(-1) in sevoflurane and desflurane treated hearts. CONCLUSION: After ischemic protection by cardioplegia, sevoflurane and desflurane given during the early reperfusion period offer additional protection against myocardial reperfusion injury.     

Cerebrovascular reactivity to carbon dioxide is preserved during hypocapnia in children anesthetized with 1.0 MAC, but not with 1.5 MAC desflurane

PURPOSE: Maintenance of cerebrovascular reactivity to CO(2) (CCO(2)R) is important during neurosurgical anesthesia. This study was designed to determine the effect of different desflurane concentrations on CCO(2)R in children. METHODS: Children undergoing urological surgery were enrolled. Anesthesia was induced with sevoflurane in air/oxygen. After intubation, sevoflurane was switched to desflurane. Analgesia was provided with an epidural neuraxial block. Mechanical ventilation was adjusted to an initial EtCO(2) of 30 mmHg. Exogenous CO(2) was used to achieve an EtCO(2) of 40 and 50 mmHg. Patients were randomized to the sequence of desflurane concentration (1.0 and 1.5 MAC) and the EtCO(2). Transcranial Doppler was used to measure middle cerebral artery blood flow velocity (Vmca). Five minutes were allowed to reach steady state after each change in EtCO(2) and 15 min after changing the desflurane concentration. RESULTS: Sixteen patients were studied. The mean age and weight were 3.5 +/- 1.5 yr and 14.4 +/- 3.1 kg, respectively. Mean arterial pressure remained stable throughout the study, while at an EtCO(2) of 50 mmHg, heart rate decreased at both desflurane concentrations (P < 0.05). At 1.0 MAC, Vmca increased from 30 to 40 mmHg (P < 0.05), but not from 40 to 50 mmHg EtCO(2). At 1.5 MAC, Vmca increased between 30 and 50 mmHg (P < 0.05). CONCLUSION: CCO(2)R is preserved during hypocapnia in children anesthetized with 1.0 MAC, but not with 1.5 MAC desflurane. The lack of further increase in Vmca at higher EtCO(2) concentrations implies that desflurane may cause significant cerebral vasodilatation in children. This may have important implications in children with reduced intracranial compliance.     

Temperatures in soda lime during degradation of desflurane, isoflurane, and sevoflurane by desiccated soda lime

Rarely, fire and patient injury result from the degradation of sevoflurane by desiccated Baralyme. The present investigation sought to determine whether high temperatures also arose with sevoflurane use in the presence of desiccated soda lime. We desiccated soda lime by directing a 10 L/min flow of oxygen through fresh absorbent. Using 1140 +/- 30 g (mean +/- sd) of this desiccated absorbent, we filled a single standard absorber canister placed in a standard anesthetic circuit to which we directed a 6 L/min flow of oxygen containing 1.5 minimum alveolar concentration (MAC) desflurane or sevoflurane, or 3.0 MAC desflurane, isoflurane, or sevoflurane (with and without concurrent delivery of 200 mL/min carbon dioxide). In an additional test, 2 canisters (rather than a single canister) containing desiccated absorbent were used and 3.0 MAC sevoflurane was applied. A 3-L reservoir bag served as a surrogate lung, and we ventilated this lung with a minute ventilation of 10 L/min. With desflurane at 1.5 MAC or 3.0 MAC or isoflurane at 3.0 MAC temperatures increased in 20 to 40 min to a peak of 30 degrees C to 45 degrees C and then declined. With 1.5 or 3.0 MAC sevoflurane, temperatures increased to approximately 90 degrees C, after which temperatures declined. Concurrent delivery of carbon dioxide and sevoflurane did not increase the peak temperatures reached. The use of 2 canisters increased the duration but not the peak of increased temperature reached with 3.0 MAC sevoflurane. No fires resulted from degradation of any anesthetic.     

Effect of the Physical Properties of Isoflurane, Sevoflurane, and Desflurane on Pulmonary Resistance in a Laboratory Lung Model

Background: Airway resistance depends not only on an airway's geometry but also on flow rate, and gas density and viscosity. A recent study showed that at clinically relevant concentrations, the mixtures of volatile agents with air and oxygen and oxygen-nitrogen affected the density of the mixture. The goal of the current study was to investigate the effect of different minimum alveolar concentrations (MACs) of three commonly used volatile agents, isoflurane, sevoflurane, and desflurane, on the measurements of airway resistance.

Methods: A two-chamber fixed-resistance test lung was connected to an anesthesia machine using the volume control mode of ventilation. Pulmonary resistance was calculated at baseline (25% oxygen in air); at 1.0, 1.5, and 2.0 MAC; and also at the same concentrations, 1.2% and 4%, of isoflurane, sevoflurane, and desflurane mixtures with 25% oxygen in air. The analysis of variance test for repeated measures and probabilities for post hoc Tukey and least significant difference tests were used.

Results: Isoflurane affected pulmonary resistance only at 2 MAC. Sevoflurane caused a significant increase of pulmonary resistance at 1.5 and 2 MAC, whereas desflurane caused the greatest increase in pulmonary resistance at all MAC values used. At 1.2% concentration, no difference from the baseline resistance was observed, whereas at 4%, the three agents produced similar increases of pulmonary resistance.     

Augmentation of the neuromuscular blocking effects of cisatracurium during desflurane, sevoflurane, isoflurane or total i.v. anaesthesia

We have evaluated the enhancement of cisatracurium-induced neuromuscular block by potent inhalation anaesthetic agents, by constructing dose-effect curves for cisatracurium in 84 patients during anaesthesia with 1.5 MAC (70% nitrous oxide) desflurane, sevoflurane, isoflurane or total i.v. anaesthesia (TIVA). Acceleromyography (TOF- Guard) and train-of-four (TOF) stimulation of the ulnar nerve were used (2 Hz every 12 s). Cisatracurium was administered in increments of 15 micrograms kg-1 until depression of T1/T0 > 95% was reached. ANOVA was used for statistical analysis (alpha = 0.05, beta = 0.2). Depression of T1/T0 during potent inhalation anaesthesia was enhanced compared with TIVA. ED50 and ED95 values of cisatracurium were 15 (SD 5) and 34 (10) micrograms kg-1 for desflurane; 15 (4) and 32 (7) micrograms kg-1 for sevoflurane; and 15 (5) and 33 (9) micrograms kg-1 for isoflurane. These were significantly lower than the values for TIVA (21 (4) and 51 (13) micrograms kg-1) (P < 0.01 in each case). After equi-effective dosing, times to T1/T0 = 25% were similar in all groups (19 (7), 19 (5), 20 (5) vs 16 (4) min). Recovery index25-75% and time to a TOF ration of 0.70 were prolonged significantly by desflurane and sevoflurane compared with TIVA (18 (5), 19 (8) vs 12 (4) min and 43 (11), 44 (10) vs 35 (5) min, respectively), whereas the difference was not significant for isoflurane (14 (6) and 41 (7) min).      

Fires from the interaction of anesthetics with desiccated absorbent

Rarely, fire and patient injury have resulted from the degradation of sevoflurane by desiccated carbon dioxide absorbent. Desiccated absorbent also can degrade desflurane and isoflurane, and in the present investigation we sought to determine whether a danger of fire also arose with their use in the presence of desiccated absorbent. Baralyme was desiccated by heating and directing a 10 L/min flow of oxygen through the absorbent. Approximately 1200 g of this desiccated absorbent was used to fill a standard absorber placed in a standard anesthetic circuit to which we directed a 6 L/min flow of oxygen containing 1.5 or 3.0 MAC desflurane, isoflurane, or sevoflurane. A 3-L reservoir bag served as a surrogate lung, and we ventilated this lung with a minute ventilation of 10 L/min. With desflurane or isoflurane, at both 1.5 MAC and 3.0 MAC, temperatures increased in 30 to 70 min to a peak of approximately 100 degrees C and then decreased. With 1.5 MAC sevoflurane (3.0 MAC was not studied), temperatures increased to over 200 degrees C, and in 2 of 5 studies, flames appeared in the anesthetic circuit. In a separate study, we found that concurrent delivery of carbon dioxide and desflurane did not increase peak temperatures. We conclude that the interaction of desflurane or isoflurane with desiccated absorbent is not likely to produce the conflagrations possible with sevoflurane.     

Pulmonary mechanics during isoflurane,sevoflurane and desflurane anaesthesia

This study was designed to investigate the effects of desflurane on bronchial smooth muscle tone, following intubation and to compare these effects with isoflurane and sevoflurane. Patients were randomly divided into three groups to receive, isoflurane (n = 22), sevoflurane (n = 23), or desflurane (n = 22). Peak inspiratory pressure (PIP), respiratory resistance (Rr) and dynamic compliance (Cdyn) measurements were recorded at three time points; After the beginning of ventilation and before inhalation agent was started, following 5 min of ventilation with 1 MAC (minimum alveolar concentration) inhalation agent and following 5 min of 2 MAC inhalation agent. We found that all inhalation agents caused a significant decrease in Peak Inspiratory Pressure (PIP) and respiratory resistance (Rr), and an increase in dynamic compliance (Cdyn) at 1 MAC concentrations. When the agent concentration was increased to 2 MAC, desflurane caused a significant increase in Rr and PIP and a decrease in Cdyn. We concluded that desflurane, like isoflurane and sevoflurane, exhibits a bronchodilator effect at 1 MAC concentration. However, increasing the concentration to 2 MAC caused an increase in airway resistance with desflurane, whilst sevoflurane and isoflurane continued to have a bronchodilator effect.     

The recovery of cognitive function after general anesthesia in elderly patients: a comparison of desflurane and sevoflurane.

We evaluated the cognitive recovery profiles in elderly patients after general anesthesia with desflurane or sevoflurane. After IRB approval, 70 ASA physical status I-III consenting elderly patients (> or =65 yr old) undergoing total knee or hip replacement procedures were randomly assigned to one of two general anesthetic groups. Propofol and fentanyl were administered for induction of anesthesia, followed by either desflurane 2%-4% or sevoflurane 1%-1.5% with nitrous oxide 65% in oxygen. The desflurane (2.5 +/- 0.6 MAC. h) and sevoflurane (2.7 +/- 0.5 MAC. h) concentrations were adjusted to maintain comparable depths of hypnosis using the electroencephalogram bispectral index monitor. The Mini-Mental State (MMS) test was used to assess cognitive function preoperatively and postoperatively at 1, 3, 6, and 24-h intervals. The use of desflurane was associated with a more rapid emergence from anesthesia (6.3 +/- 2.4 min versus 8.0 +/- 2.8 min) and a shorter length of stay in the postanesthesia care unit (213 +/- 66 min versus 241 +/- 87 min). However, there were no significant differences between the Desflurane and the Sevoflurane groups when the MMS scores were compared preoperatively, and postoperatively at 1, 3, 6, and 24 h. Compared with the preoperative (baseline) MMS scores, the values were significantly decreased at 1 h postoperatively (27.8 +/- 1.7 versus 29.5 +/- 0.5 in the Desflurane group, and 27.4 +/- 1.7 versus 29.2 +/- 1.0 in the Sevoflurane group, respectively). However, the MMS scores returned to preoperative baseline levels within 6 h after surgery. At 1 h and 3 h after surgery, 51% and 11% (versus 57% and 9%) of patients in the Desflurane (versus Sevoflurane) Group experienced cognitive impairment. In conclusion, desflurane is associated with a faster early recovery than sevoflurane after general anesthesia in elderly patients. However, recovery of cognitive function was similar after desflurane and sevoflurane-based anesthesia. IMPLICATIONS: Desflurane was associated with a faster early recovery than sevoflurane after general anesthesia in elderly patients. However, recovery of cognitive function was similar with both volatile anesthetics.     

Sevoflurane increases lumbar cerebrospinal fluid pressure in normocapnic patients undergoing transsphenoidal hypophysectomy.

BACKGROUND: The data on the effect of sevoflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that sevoflurane would increase intracranial pressure as compared to propofoL METHODS: In 20 patients with no evidence of mass effect undergoing transsphenoidal hypophysectomy, anesthesia was induced with intravenous fentanyl and propofol and maintained with 70% nitrous oxide in oxygen and a continuous propofol infusion, 100 microg x kg(-1) x min(-1). The authors assigned patients to two groups randomized to receive only continued propofol infusion (n = 10) or sevoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the sevoflurane group received, in random order, two concentrations (0.5 times the minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of sevoflurane for 10 min each. The authors continuously monitored lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations. RESULTS: Lumbar CSF pressure increased by 2+/-2 mmHg (mean+/-SD) with both 0.5 MAC and 1 MAC of sevoflurane. Cerebral perfusion pressure decreased by 11+/-5 mmHg with 0.5 MAC and by 15+/-4 mmHg with 1.0 MAC of sevoflurane. Systolic blood pressure decreased with both concentrations of sevoflurane. To maintain blood pressure within predetermined limits (within+/-20% of baseline value), phenylephrine was administered to 5 of 10 patients in the sevoflurane group (range = 50-300 microg) and no patients in the propofol group. Lumbar CSF pressure, cerebral perfusion pressure, and systolic blood pressure did not change in the propofol group. CONCLUSIONS: Sevoflurane, at 0.5 and 1.0 MAC, increases lumbar CSF pressure. The changes produced by 1.0 MAC sevoflurane did not differ from those observed in a previous study with 1.0 MAC isoflurane or desflurane.     

The cerebral functional, metabolic, and hemodynamic effects of desflurane in dogs

The effects of 0.5-2.0 MAC (3.6-15%) desflurane on cerebral function, metabolism, and hemodynamics and on systemic metabolism and hemodynamics were examined in dogs. Desflurane produced a significant dose-related decrease in cerebral vascular resistance from 1.53 +/- 0.21 mmHg.ml-1.min.100 g at 0.5 MAC to 0.50 +/- 0.03 mmHg.ml-1.min.100 g at 2.0 MAC desflurane. This was accompanied by an increase in cerebral blood flow (CBF) from 61 +/- 7 ml.min-1.100 g-1 at 0.5 MAC to 78 +/- 3 ml.min-1.100 g-1 at 1.5 MAC desflurane. At 2.0 MAC desflurane CBF was 52 +/- 2 ml.min-1.100 g-1 but was associated with a decrease in mean arterial pressure (MAP) to 43 +/- 2 mmHg. When MAP was increased to 73 +/- 3 mmHg with phenylephrine, CBF increased to 87 +/- 3 ml.min-1.100 g-1 at this concentration. At 0.5 MAC desflurane, intracranial pressure (ICP) was 15 +/- 5 mmHg, higher than normal, but did not change significantly with increasing concentrations of desflurane. Increasing concentrations of desflurane initially produced on the EEG the common pattern sequence of increasing depth of anesthesia with decreasing frequency and increasing amplitude progressing to burst suppression and then at 2.0 MAC desflurane to regular attenuation with interruption by periodic polyspiking, a pattern similar to that seen with isoflurane. At both 1.5 and 2.0 MAC the EEG pattern initially observed at that concentration changed to one with faster background activity with time.(ABSTRACT TRUNCATED AT 250 WORDS)     

Desflurane and Isoflurane Increase Lumbar Cerebrospinal Fluid Pressure in Normocapnic Patients Undergoing Transsphenoidal Hypophysectomy

Background: Rapid emergence from anesthesia makes desflurane an attractive choice as an anesthetic for patients having neurosurgery. However, the data on the effect of desflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that isoflurane and desflurane increase intracranial pressure compared with propofol.

Methods: Anesthesia was induced with intravenous fentanyl and propofol in 30 patients having transsphenoidal hypophysectomy with no evidence of mass effect, and it was maintained with 70% nitrous oxide in oxygen and a continuous 100 micro gram [centered dot] kg sup -1 [centered dot] min sup -1 infusion of propofol. Patients were assigned to three groups randomized to receive only continued propofol infusion (n = 10), desflurane (n = 10), or isoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the desflurane and isoflurane groups received, in random order, two concentrations (0.5 minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of desflurane or isoflurane for 10 min each. Lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations were monitored continuously.

Results: Lumbar CSF pressure increased significantly in all patients receiving desflurane or isoflurane. Lumbar CSF pressure increased by 5 +/- 3 mmHg at 1-MAC concentrations of desflurane and by 4 +/- 2 mmHg at 1-MAC concentrations of isoflurane. Cerebral perfusion pressure decreased by 12 +/- 10 mmHg at 1-MAC concentrations of desflurane and by 15 +/- 10 mmHg at 1-MAC concentrations of isoflurane. Heart rate increased by 7 +/- 9 bpm with 0.5 MAC desflurane and by 8 +/- 7 bpm with 1.0 MAC desflurane, and by 5 +/- 11 bpm with 1.0 MAC isoflurane. Systolic blood pressure decreased in all but the patients receiving 1.0 MAC desflurane. To maintain blood pressure within predetermined limits, phenylephrine was administered to six of ten patients in the isoflurane group (range, 25 to 600 micro gram), two of ten patients in the desflurane group (range, 200 to 500 micro gram), and in no patients in the propofol group. Lumbar CSF pressure, heart rate, and systolic blood pressure did not change in the propofol group.