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.     

Carbon monoxide production from sevoflurane breakdown: modeling of exposures under clinical conditions

Isoflurane, enflurane, sevoflurane, and especially desflurane produce carbon monoxide (CO) during reaction with desiccated absorbents. Of these, sevoflurane is the least studied. We investigated the dependence of CO production from sevoflurane on absorbent temperature, minute ventilation (VE), and fresh gas flow rates. We measured absorbent temperature and in vitro CO concentrations when desiccated Baralyme reacted with 1 minimum alveolar anesthetic concentration of (2.1%) sevoflurane at 2.3-, 5.0-, and 10.0-L VE. Mathematical modeling of carboxyhemoglobin concentrations was performed using an existing iterative method. Rapid breakdown of sevoflurane prevented the attainment of 1 minimum alveolar anesthetic concentration with low fresh gas flow rates. CO concentrations increased with VE and with absorbent temperatures exceeding 80 degrees C, but concentrations decreased with higher fresh gas flow rates. Average CO concentrations were 150 and 600 ppm at 2.3- and 5.0-L VE; however, at 10 L, over 11,000 ppm of CO were produced followed by an explosion and fire. Methanol and formaldehyde were present and may have contributed to the flammable mixture but were not quantitated. Mathematical modeling of exposures indicates that in average cases, only patients < or =25 kg, or severely anemic patients, are at risk of carboxyhemoglobin concentrations >10% during the first 60 min of anesthesia. IMPLICATIONS: Sevoflurane breakdown in desiccated absorbents is expected to result in only mild carbon monoxide (CO) exposure. Completely dry absorbent and high minute ventilation rates may degrade sevoflurane to extremely large CO concentrations. Serious CO poisoning or spontaneous ignition of flammable gases within the breathing circuit are possible in extreme circumstances.     

Physical Factors Affecting the Production of Carbon Monoxide from Anesthetic Breakdown

Background: Parameters determining carbon monoxide (CO) concentrations produced by anesthetic breakdown have not been adequately studied in clinical situations. The authors hypothesized that these data will identify modifiable risk factors.

Methods: Carbon monoxide concentrations were measured when partially desiccated barium hydroxide lime was reacted with isoflurane (1.5%) and desflurane (7.5%) in a Draeger Narkomed 2 anesthesia machine with a latex breathing bag substituting for a patient. Additional experiments determined the effects of carbon dioxide (0 or 350 ml/min), fresh gas flow rates (1 or 4 l/min), minute ventilation (6 or 18 l/min), or absorbent quantity (1 or 2 canisters). End-tidal anesthetic concentrations were adjusted according to a monochromatic infrared monitor.

Results: Desflurane produced approximately 20 times more CO than isoflurane when completely dried absorbents were used. Peak CO concentrations approached 100,000 ppm with desflurane. Traces of water remaining after a 66-h drying time (one weekend) markedly reduced the generation of CO compared with 2 weeks of drying. Reducing the quantity of desiccated absorbent by 50% reduced the total CO production by 40% in the first hour. Increasing the fresh gas flow rate from 1 to 4 l/min increased CO production by 67% in the first hour but simultaneously decreased average inspiratory concentrations by 53%. Carbon dioxide decreased CO production by 12% in completely desiccated absorbents.     

Physical factors affecting the production of carbon monoxide from anesthetic breakdown

BACKGROUND: Parameters determining carbon monoxide (CO) concentrations produced by anesthetic breakdown have not been adequately studied in clinical situations. The authors hypothesized that these data will identify modifiable risk factors. METHODS: Carbon monoxide concentrations were measured when partially desiccated barium hydroxide lime was reacted with isoflurane (1.5%) and desflurane (7.5%) in a Draeger Narkomed 2 anesthesia machine with a latex breathing bag substituting for a patient. Additional experiments determined the effects of carbon dioxide (0 or 350 ml/min), fresh gas flow rates (1 or 4 l/min), minute ventilation (6 or 18 l/min), or absorbent quantity (1 or 2 canisters). End-tidal anesthetic concentrations were adjusted according to a monochromatic infrared monitor. RESULTS: Desflurane produced approximately 20 times more CO than isoflurane when completely dried absorbents were used. Peak CO concentrations approached 100,000 ppm with desflurane. Traces of water remaining after a 66-h drying time (one weekend) markedly reduced the generation of CO compared with 2 weeks of drying. Reducing the quantity of desiccated absorbent by 50% reduced the total CO production by 40% in the first hour. Increasing the fresh gas flow rate from 1 to 4 l/min increased CO production by 67% in the first hour but simultaneously decreased average inspiratory concentrations by 53%. Carbon dioxide decreased CO production by 12% in completely desiccated absorbents. CONCLUSION: Anesthetic identity, fresh gas flow rates, absorbent quantity, and water content are the most important factors determining patient exposures. Minute ventilation and carbon dioxide production by the patient are relatively unimportant.     

Mechanistic Aspects of Carbon Monoxide Formation from Volatile Anesthetics

Background: Desflurane, enflurane and isoflurane can be degraded to carbon monoxide (CO) by carbon dioxide absorbents, whereas sevoflurane and halothane form negligible amounts of CO. Carbon monoxide formation is greater with drier absorbent, and with barium hydroxide, than with soda lime. The mechanism, role of absorbent composition and water, and anesthetic structures determining CO formation are unknown. This investigation examined sequential steps in anesthetic degradation to CO.

Methods: Carbon monoxide formation from anesthetics and desiccated barium hydroxide lime or soda lime was determined at equimole from deuterium-substituted anesthetics was also quantified. Proton abstraction from anesthetics by strong base was determined by deuterium isotope exchange. A reactive chemical intermediate was trapped and identified by gas chromatography-mass spectrometry. The source of the oxygen in CO was identified by18 O incorporation.

Results: Desflurane, enflurane, and isoflurane (difluoromethylethyl ethers), but not sevoflurane (monofluoromethyl ether), methoxyflurane (methyl-ethyl ether), or halothane (alkane) were degraded to CO. The amount of CO formed was desflurane >or= to enflurane > isoflurane at equiMAC and enflurane > desflurane > isoflurane at equimole concentrations. Proton abstraction from the difluoromethoxy carbon was greater with potassium than with sodium hydroxide, but unmeasurable with barium hydroxide. Carbon monoxide formation was correlated (r = 0.95-1.00) with difluoromethoxy (enflurane > desflurane > isoflurane >or= to methoxyflurane = sevoflurane = 0) but not ethyl carbon proton abstraction. Deuterium substitution on enflurane and desflurane diminished CO formation. Chemical trapping showed formation of a difluorocarbene intermediate from enflurane and desflurane. Incorporation of H218 O in barium hydroxide lime resulted in C18 O formation from unlabeled enflurane and desflurane.     

Low-flow anesthesia and reduced animal size increase carboxyhemoglobin levels in swine during desflurane and isoflurane breakdown in dried soda lime

After institutional approval, we studied the effect of animal size, anesthetic concentration, and fresh gas flow (FGF) rate on inspired carbon monoxide (CO) and carboxyhemoglobin (COHb) during anesthesia in swine, using soda lime previously dried to 1 +/- 0.1% water content. To ascertain the effect of anesthesia, eight adult pigs were anesthetized with either 1 minimum alveolar anesthetic concentration (MAC) desflurane or isoflurane and, to characterize the effect of the FGF rate, it was doubled in four pigs. To determine the effect of animal size, four small and four large pigs received 1 MAC desflurane or isoflurane, and to determine the effect of the anesthetic concentration, a group of four swine was exposed to 0.5 MAC. CO and COHb concentrations were larger with desflurane (5500 +/- 980 ppm and 57.90% +/- 0.50%, respectively) than with isoflurane (800 ppm and 17.8% +/- 2.14%, respectively), especially in the small animals. Increasing the FGF rate significantly reduced peak CO and COHb concentrations resulting from both anesthetics; however, when each anesthetic was reduced to 0.5 MAC, the concentrations obtained were similar. We conclude that CO intoxication is more severe with desflurane than with isoflurane, that small animals are at higher risk for CO poisoning, and that low FGF can increase COHb concentrations. IMPLICATIONS: The present study shows that the use of desflurane with desiccated carbon dioxide absorbents in pediatric anesthesia can produce a dangerous carbon dioxide intoxication, especially with low-flow anesthesia.     

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     

Comparison of Amsorb, sodalime, and Baralyme degradation of volatile anesthetics and formation of carbon monoxide and compound a in swine in vivo.

BACKGROUND: Consequences of volatile anesthetic degradation by carbon dioxide absorbents that contain strong base include formation of compound A from sevoflurane, formation of carbon monoxide (CO) and CO toxicity from desflurane, enflurane and isoflurane, delayed inhalation induction, and increased anesthetic costs. Amsorb (Armstrong Ltd., Coleraine, Northern Ireland) is a new absorbent that does not contain strong base and does not form CO or compound A in vitro. This investigation compared Amsorb, Baralyme (Chemetron Medical Division, Allied Healthcare Products, St. Louis, MO), and sodalime effects on CO (from desflurane and isoflurane) and compound A formation, carboxyhemoglobin (COHb) concentrations, and anesthetic degradation in a clinically relevant porcine in vivo model. METHODS: Pigs were anesthetized with desflurane, isoflurane, or sevoflurane, using fresh or partially dehydrated Amsorb, Baralyme, and new and old formulations of sodalime. Anesthetic concentrations in the fresh (preabsorber), inspired (postabsorber), and end-tidal gas were measured, as were inspired CO and compound A concentrations and blood oxyhemoglobin and COHb concentrations. RESULTS: For desflurane and isoflurane, the order of inspired CO and COHb formation was dehydrated Baralyme > soda-lime > Amsorb. For desflurane and Baralyme, peak CO was 9,700 +/- 5,100 parts per million (ppm), and the increase in COHb was 37 +/- 14%. CO and COHb increases were undetectable with Amsorb. Oxyhemoglobin desaturation occurred with desflurane and Baralyme but not Amsorb or sodalime. The gap between inspired and end-tidal desflurane and isoflurane did not differ between the various dehydrated absorbents. Neither fresh nor dehydrated Amsorb caused compound A formation from sevoflurane. In contrast, Baralyme and sodalime caused 20-40 ppm compound A. The gap between inspired and end-tidal sevoflurane did not differ between fresh absorbents, but was Amsorb < sodalime < Baralyme with dehydrated absorbents. CONCLUSION: Amsorb caused minimal if any CO formation, minimal compound A formation regardless of absorbent hydration, and the least amount of sevoflurane degradation. An absorbent like Amsorb, which does not contain strong base or cause anesthetic degradation and formation of toxic products, may have benefit with respect to patient safety, inhalation induction, and anesthetic consumption (cost).     

Comparative pharmacodynamic modeling of the electroencephalography-slowing effect of isoflurane, sevoflurane, and desflurane.

BACKGROUND: The most common measure to compare potencies of volatile anesthetics is minimum alveolar concentration (MAC), although this value describes only a single point on a quantal concentration-response curve and most likely reflects more the effects on the spinal cord rather than on the brain. To obtain more complete concentration-response curves for the cerebral effects of isoflurane, sevoflurane, and desflurane, the authors used the spectral edge frequency at the 95th percentile of the power spectrum (SEF95) as a measure of cerebral effect. METHODS: Thirty-nine patients were randomized to isoflurane, sevoflurane, or desflurane groups. After induction with propofol, intubation, and a waiting period, end-tidal anesthetic concentrations were randomly varied between 0.6 and 1.3 MAC, and the EEG was recorded continuously. Population pharmacodynamic modeling was performed using the software package NONMEM. RESULTS: The population mean EC50 values of the final model for SEF95 suppression were 0.66+/-0.08 (+/- SE of estimate) vol% for isoflurane, 1.18+/-0.10 vol% for sevoflurane, and 3.48+/-0.66 vol% for desflurane. The slopes of the concentration-response curves were not significantly different; the common value was lambda = 0.86+/-0.06. The Ke0 value was significantly higher for desflurane (0.61+/-0.11 min(-1)), whereas separate values for isoflurane and sevoflurane yielded no better fit than the common value of 0.29+/-0.04 min(-1). When concentration data were converted into fractions of the respective MAC values, no significant difference of the C50 values for the three anesthetic agents was found. CONCLUSIONS: This study demonstrated that (1) the concentration-response curves for spectral edge frequency slowing have the same slope, and (2) the ratio C50(SEF95)/MAC is the same for all three anesthetic agents. The authors conclude that MAC and MAC multiples, for the three volatile anesthetics studied, are valid representations of the concentration-response curve for anesthetic suppression of SEF95.     

地氟醚、七氟醚和异氟醚预处理对缺氧/复氧心肌细胞损害的保护作用

目的　研究地氟醚、七氟醚和异氟醚预处理对心肌细胞缺氧／复氧损害的保护作用。方法　原代培养乳鼠心肌细胞，随机分为对照、单纯缺氧／复氧及 １．５ＭＡＣ地氟醚、七氟醚和异氟醚预处理５组。实验结束测定乳酸脱氢酶（ＬＤＨ）和肌酸激酶（ＣＫ）活性、细胞存活和凋亡率。结果　与对照组比，单纯缺氧／复氧使ＬＤＨ、ＣＫ和细胞凋亡率升高及细胞存活率显著下降（Ｐ＜０．０１）；１．５ＭＡＣ地氟醚、七氟醚和异氟醚预处理显著减轻ＬＤＨ、ＣＫ和细胞凋亡率升高及细胞存活率下降，其中七氟醚减轻作用最强。结论　地氟醚、七氟醚和异氟醚预处理对心肌细胞缺氧／复氧损害有一定的保护作用，七氟醚的保护作用可能更强。     

Minimum alveolar anesthetic concentration of volatile anesthetics in normal and cardiomyopathic hamsters

Minimum alveolar anesthetic concentrations (MAC) values of volatile anesthetics in cardiovascular diseases remain unknown. We determined MAC values of volatile anesthetics in spontaneously breathing normal and cardiomyopathic hamsters exposed to increasing (0.1%-0.3% steps) concentrations of halothane, isoflurane, sevoflurane, or desflurane (n = 30 in each group) using the tail-clamp technique. MAC values and their 95% confidence interval were calculated using logistic regression. In normal hamsters, inspired MAC values were: halothane 1.15% (1.10%-1.20%), isoflurane 1.62% (1.54%-1.69%), sevoflurane 2.31% (2.22%-2.40%), and desflurane 7.48% (7.30%-7.67%). In cardiomyopathic hamsters, they were: halothane 0.89% (0.83%-0.95%), isoflurane 1.39% (1.30%-1.47%), sevoflurane 2.00% (1.85%-2.15%), and desflurane 6.97% (6.77%-7.17%). Thus, MAC values of halothane, isoflurane, sevoflurane, and desflurane were reduced by 23% (P < 0.05), 14% (P < 0.05), 13% (P < 0.05), and 7% (P < 0.05), respectively in cardiomyopathic hamsters. IMPLICATIONS: Minimum alveolar anesthetic concentrations of volatile anesthetics were significantly lower in cardiomyopathic hamsters than in normal hamsters.     

Mathematical Modeling of Carbon Monoxide Exposures from Anesthetic Breakdown: Effect of Subject Size, Hematocrit, Fraction of Inspired Oxygen, and Quantity of Carbon Monoxide

Background: Carbon monoxide (CO) is produced by reaction of isoflurane, enflurane, and desflurane in desiccated carbon dioxide absorbents. The inspiratory CO concentration depends on the dryness and identity of the absorbent and anesthetic. The adaptation of existing mathematical models to a rebreathing circuit allows identification of patient factors that predispose to more severe exposures, as identified by carboxyhemoglobin concentration.

Methods: From our companion study, the authors used quantitative in vitro CO production data for 60 min at 7.5% desflurane or 1.5% isoflurane at 1 l/min fresh gas flow. The carboxyhemoglobin concentration was calculated by iteratively solving the Coburn Forster Kane equation modified for a rebreathing system that incorporates the removal of CO by patient absorption. Demonstrating good fit of predicted carboxyhemoglobin concentrations to published data from animal and human exposures validated the model. Carboxyhemoglobin concentrations were predicted for exposures of various severity, patients of different sizes, hematocrit, and fraction of inspired oxygen.

Results: The calculated carboxyhemoglobin concentrations closely predicted the experimental results of other investigators, thereby validating the model. These equations indicate the severity of CO poisoning is inversely related to the hemoglobin quantity of a subject. Fraction of inspired oxygen had the greatest effect in patients of small size with low hematocrit values, where equilibrium and not the rate of uptake determined carboxyhemoglobin concentrations.     

Comparative Pharmacodynamic Modeling of the Electroencephalography-slowing Effect of Isoflurane, Sevoflurane, and Desflurane

Background: The most common measure to compare potencies of volatile anesthetics is minimum alveolar concentration (MAC), although this value describes only a single point on a quantal concentration-response curve and most likely reflects more the effects on the spinal cord rather than on the brain. To obtain more complete concentration-response curves for the cerebral effects of isoflurane, sevoflurane, and desflurane, the authors used the spectral edge frequency at the 95th percentile of the power spectrum (SEF95) as a measure of cerebral effect.

Methods: Thirty-nine patients were randomized to isoflurane, sevoflurane, or desflurane groups. After induction with propofol, intubation, and a waiting period, end-tidal anesthetic concentrations were randomly varied between 0.6 and 1.3 MAC, and the EEG was recorded continuously. Population pharmacodynamic modeling was performed using the software package NONMEM.

Results: The population mean EC50 values of the final model for SEF (95) suppression were 0.66 +/- 0.08 (+/- SE of estimate) vol% for isoflurane, 1.18 +/- 0.10 vol% for sevoflurane, and 3.48 +/- 0.66 vol% for desflurane. The slopes of the concentration-response curves were not significantly different; the common value was [Greek small letter lambda] = 0.86 +/- 0.06. The Ke0 value was significantly higher for desflurane (0.61 +/- 0.11 min-1), whereas separate values for isoflurane and sevoflurane yielded no better fit than the common value of 0.29 +/- 0.04 min (-1). When concentration data were converted into fractions of the respective MAC values, no significant difference of the C50 values for the three anesthetic agents was found.     

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.     

Effect of fentanyl and nitrous oxide on the desflurane anesthetic requirement

The minimum alveolar anesthetic concentration (MAC) of desflurane (I-653) was determined when administered with 60% nitrous oxide (N2O) in oxygen after a standardized induction sequence consisting of 0, 3, 6, or 9 micrograms/kg intravenous (IV) fentanyl followed by 3-6 mg/kg IV thiopental and 1.5 mg/kg IV succinylcholine. For comparison, we also determined the isoflurane MAC with 60% N2O in oxygen after an induction dose of 3 micrograms/kg IV fentanyl and similar doses of thiopental and succinylcholine. All patients were undergoing elective surgical procedures. The minimum alveolar anesthetic concentration in patients given isoflurane and 60% N2O with 3 micrograms/kg fentanyl was 0.4%, approximately 20% below previously reported MAC values for isoflurane with 60% N2O alone. The minimum alveolar anesthetic concentration of desflurane with 60% N2O plus 0, 3, 6, and 9 micrograms/kg IV fentanyl was 3.7%, 3.0%, 1.2%, and 0.1%, respectively. Thus, the MAC-lowering effect of 3 micrograms/kg IV fentanyl appears to be similar with both isoflurane and desflurane. Fentanyl, 3-9 micrograms/kg IV, produces dose-dependent decreases in the MAC of desflurane.     

Changing from Isoflurane to Desflurane toward the End of Anesthesia Does Not Accelerate Recovery in Humans

Background: In an attempt to combine the advantage of the lower solubilities of new inhaled anesthetics with the lesser cost of older anesthetics, some clinicians substitute the former for the latter toward the end of anesthesia. The authors tried to determine whether substituting desflurane for isoflurane in the last 30 min of a 120-min anesthetic would accelerate recovery.

Methods: Five volunteers were anesthetized three times for 2 h using a fresh gas inflow of 2 l/min: 1.25 minimum alveolar concentration (MAC) desflurane, 1.25 MAC isoflurane, and 1.25 MAC isoflurane for 90 min followed by 30 min of desflurane concentrations sufficient to achieve a total of 1.25 MAC equivalent ("crossover"). Recovery from anesthesia was assessed by the time to respond to commands, by orientation, and by tests of cognitive function.

Results: Compared with isoflurane, the crossover technique did not accelerate early or late recovery (P > 0.05). Recovery from isoflurane or the crossover anesthetic was significantly longer than after desflurane (P < 0.05). Times to response to commands for isoflurane, the crossover anesthetic, and desflurane were 23 +/- 5 min (mean +/- SD), 21 +/- 5 min, and 11 +/- 1 min, respectively, and to orientation the times were 27 +/- 7 min, 25 +/- 5 min, and 13 +/- 2 min, respectively. Cognitive test performance returned to reference values 15-30 min sooner after desflurane than after isoflurane or the crossover anesthetic. Isoflurane cognitive test performance did not differ from that with the crossover anesthetic at any time.     

Rehydration of Desiccated Baralyme Prevents Carbon Monoxide Formation from Desflurane in an Anesthesia Machine

Background: Desiccated carbon dioxide absorbents degrade desflurane, enflurane, and isoflurane to carbon monoxide (CO) in vitro and in anesthesia machines, which can result in significant clinical CO exposure. Carbon monoxide formation is highest from desflurane, and greater with Baralyme than with soda lime. Degradation is inversely related to absorbent water content, and thus the greatest CO concentrations occur with desflurane and fully desiccated Baralyme. This investigation tested the hypothesis that rehydrating desiccated absorbent can diminish CO formation.

Methods: Baralyme was dried to constant weight. Carbon monoxide formation from desflurane and desiccated Baralyme was determined in sealed 20.7-ml vials without adding water, after adding 10% of the normal water content (1.3% water), and after adding 100% of the normal water content (13% water) to the dry absorbent. Similar measurements were made using an anesthesia machine and circle system. Carbon monoxide was measured by gas chromatography-mass spectrometry.

Results: Carbon monoxide formation from desflurane in vitro was decreased from 10,700 ppm with desiccated Baralyme to 715 ppm and less than 100 ppm, respectively, when 1.3% and 13% water were added. Complete rehydration also decreased CO formation from enflurane and isoflurane to undetectable concentrations. Desflurane degradation in an anesthesia machine produced 2,500 ppm CO in the circuit, which was reduced to less than 180 ppm when the full complement of water (13%) was added to the dried absorbent.     

Influence of 0.1 minimum alveolar concentration of sevoflurane, desflurane and isoflurane on dynamic ventilatory response to hypercapnia in humans

To assess the effects and site of action of a sub-anaesthetic concentration of isoflurane, desflurane and sevoflurane (0.1 minimum alveolar concentration (MAC)) on respiratory control, we measured the ventilatory response to square wave changes in PE1CO2 against a background of normoxia. Using the computer steered "end-tidal forcing system", 2 min of steady state ventilation were followed by a step increase in PE1CO2 (1-1.5 kPa). This level was maintained for 8 min, followed by a step decrease to the original value for another 8 min. Each hypercapnic response was separated into a fast, peripheral component and a slow, central component, characterized by a time constant, carbon dioxide sensitivity, time delay and off-set. We studied 25 healthy volunteers; they performed 2-3 studies without and 2- 3 studies during inhalation of the anaesthetic agent. Level of sedation was scored using a subjective seven-point scale from 0 (= alert and awake) to 6 (unrousable). In the isoflurane (16 subjects, 33 control, 37 drug studies) and sevoflurane (15 subjects, 40 control, 41 drug studies) studies, peripheral carbon dioxide sensitivity was reduced by approximately 45% and approximately 27% (ANOVA, P < 0.05 vs control), respectively, without affecting central carbon dioxide sensitivity or apnoeic threshold. In the desflurane study (16 subjects, 36 control, 37 drug studies), no significant effect was observed for any of the variables measured. A significant relation was observed between sedation score and change from control in central carbon dioxide sensitivities in the isoflurane and desflurane studies and in the change in the ratio peripheral carbon dioxide sensitivity over total carbon dioxide sensitivity in the sevoflurane studies. At the highest level of sedation observed (score 3-arousal state comparable with "light sleep"--in three subjects) these latter variables differed significantly from those in the other observed sedation levels (scores 1 and 2-a state of drowsiness). We conclude that 0.1 MAC of isoflurane and sevoflurane depressed the peripheral chemoreflex loop, without affecting the central chemoreflex loop. Desflurane at the same MAC showed no effect on peripheral and central carbon dioxide sensitivity. When the level of sedation was considered, our data suggested that at levels of sedation comparable with sleep, a depressive effect of all three anaesthetics was observed on the central chemoreflex loop.      

Immediate anesthesia recovery and psychomotor function of patient after prolonged anesthesia with desflurane, sevoflurane or isoflurane

OBJECTIVE: To compare the anesthetic maintenance and early postoperative recovery and psychomotor function in patients who have been anesthestized with desflurane, sevoflurane or isoflurane during prolonged open urological surgery. PATIENTS AND METHODS: Seventy-five patients were randomly assigned to receive desflurane, sevoflurane or isoflurane with N2O 60% for anesthetic maintenance. The concentration of each drug was adjusted to maintain arterial pressure and heart rate +/- 20% of baseline. After the operation the anesthetics were discontinued and times until eye opening, spontaneous breathing, extubation and orientation were recorded. In the post-anesthesia recovery ward we applied the Newman-Trieger and Aldrete tests and recorded instances of nausea and vomiting and need for analgesia during the first 24 hours after surgery. RESULTS: The groups were similar with regard to demographic features, anesthetic maintenance, duration of anesthesia and relative doses of the anesthetics used. Recovery times in the operating room were significantly shorter (p < 0.05) after anesthesia with desflurane and sevoflurane than with isoflurane, with no significant differences between the desflurane and sevoflurane groups (duration of anesthesia 198 +/- 90, 171 +/- 67 and 191 +/- 79; eye opening 7.6 +/- 3.7, 7.8 +/- 3.0 and 11.9 +/- 4.5; time until extubation 7.8 +/- 3.0, 8.3 +/- 3.0 and 11.0 +/- 3.5 for desflurane, sevoflurane and isoflurane, respectively; all data in minutes). Recovery in the post-anesthetic recovery ward was similar for all three groups. CONCLUSIONS: Anesthetic maintenance was comparable with all three drugs. Desflurane and sevoflurane demonstrated advantages over isoflurane during recovery from anesthesia in the operating theater. No significant differences were found in psychomotor recovery, nausea and/or vomiting or requirements for postoperative analgesia.     

Newer inhalation anaesthetics and neuro-anaesthesia: what is the place for sevoflurane or desflurane?

The effects on cerebral circulation and metabolism of sevoflurane and desflurane are largely comparable to isoflurane. Both induce a direct vasodilation of the cerebral vessels, resulting in a less pronounced decrease in cerebral blood flow compared to the decrease in cerebral metabolism. This direct vasodilation seems to be dose-dependent and more pronounced for desflurane > isoflurane > sevoflurane. Many reports suggest luxury perfusion at high concentrations of desflurane. Sevoflurane maintains intact cerebral autoregulation up to 1.5 MAC. Desflurane induces a significant impairment in autoregulation, with a completely abolished autoregulation at 1.5 MAC. Both sevoflurane and desflurane (up to 1.5 MAC) maintain normal CO(2) regulation. As to their effect on final intracranial pressure (ICP), both sevoflurane and desflurane revealed no increases in ICP. However, compared to intravenous hypnotics, subdural ICP is higher with volatiles because of their tendency to increase cerebral swelling after dura opening (isoflurane > sevoflurane). Several case reports have noted seizure-like movements, as well as EEG recorded seizures during induction of sevoflurane anesthesia. Especially, in children during inhalational induction with hyperventilation at a high sevoflurane concentration, severe epileptiform EEG with a hyperdynamic response were observed, which urges for caution using inhalational sevoflurane induction in children for neurosurgical procedures. Neuroprotective properties (reduced neuronal death either by necrosis or apoptosis) have been attributed to all volatile agents. However, these neuroprotective effects have been described in experimental or animal models, so their possible effect on humans remains to be proven.