Comparison of induction, maintenance, and recovery characteristics of sevoflurane-N2O and propofol-sevoflurane-N2O with propofol-isoflurane-N2O anesthesia.

Induction of, maintenance of, and recovery from sevoflurane anesthesia were compared with propofol and isoflurane anesthesia when administered with nitrous oxide to patients undergoing gynecologic surgery. Seventy-five healthy (ASA I or II), consenting patients were randomly assigned to receive either (I) propofol for induction of anesthesia and isoflurane-nitrous oxide for maintenance (control), (II) propofol for induction and sevoflurane-nitrous oxide for maintenance, or (III) sevoflurane-nitrous oxide for induction and maintenance of anesthesia. Inhaled induction of anesthesia with sevoflurane-nitrous oxide was rapid (109 +/- 25 s to loss of consciousness) and without any untoward hemodynamic changes or episodes of coughing and laryngospasm. Mean arterial blood pressure after induction of anesthesia with propofol (71 +/- 11, 73 +/- 12 mm Hg for groups I and II, respectively) was lower than when sevoflurane (80 +/- 14 mm Hg) was used. The emergence time after discontinuation of isoflurane-nitrous oxide (6.7 +/- 2.2 min) was significantly longer than after propofol-sevoflurane-nitrous oxide or sevoflurane-nitrous oxide alone (4.1 +/- 2.2 and 4.0 +/- 2.0 min for groups II and III, respectively). However, later recovery events did not differ between groups. Serum fluoride levels increased after administration of sevoflurane but not isoflurane. The levels of fluoride ions correlated with the degree of exposure to sevoflurane in MAC-hours. In conclusion, induction of anesthesia with either propofol or sevoflurane-nitrous oxide was rapid and without significant side effects. Emergence and early recovery after maintenance of anesthesia with sevoflurane-nitrous oxide was significantly faster than that after an isoflurane-nitrous oxide combination.     

Stress hormone responses to major intra-abdominal surgery during and immediately after sevoflurane-nitrous oxide anaesthesia in elderly patients

We studied the responses of plasma epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), cortisol, and antidiuretic hormone (ADH) during and immediately after sevoflurane-nitrous oxide anaesthesia supplemented with vecuronium in seven elderly patients (mean 76.6 ± 1.7 SEM) who underwent major intra-abdominal surgery. The plasma concentrations of norepinephrine, ACTH, cortisol, and ADH increased in response to surgical procedures (P <0.05). The plasma concentration of ADH increased to a peak concentration of 189.1 ± 20.7 pg · ml^?1 30 min after skin incision (P < 0.05). the plasma concentrations of epinephrine, norepinephrine, ACTH, and cortisol increased to peak concentrations of 408.6 ± 135.5 pg · ml^?1, 635.7 ± 167.8 pg · ml^?1, 222.6 ± 48.0 pg · ml^?1, and 113.6 ± 67.5 μg · dI^?1, respectively immediately after tracheal extubation (P <0.05). We conclude that, in the elderly patients, the responses of stress hormones to major intraabdominal surgery were preserved during sevoflurane-nitrous oxide anaesthesia sufficient to prevent increases in arterial pressure and heart rate. The strongest responses of epinephrine, norepinephrine, ACTH, and cortisol were elicited immediately after treacheal extubation.     

Hemodynamic and catecholamine response to a rapid increase in isoflurane or sevoflurane concentration during a maintenance phase of anesthesia in humans

Purpose The purpose of this study was to compare hemodynamic and catecholamine changes due to a sudden increase in inhalation anesthetic concentrations (isoflurane and sevoflurane) during surgery.Methods Thirty patients aged 40–70 years scheduled for lower abdominal surgery were anesthetized with either isoflurane or sevoflurane with nitrous oxide and epidural block. During surgery the isoflurane or sevoflurane concentration was kept at 0.5 minimum alveolar concentration (MAC) (end-tidal concentration) for 15 min. Then the isoflurane or sevoflurane concentration (inhalation concentration) was changed to 1.5 MAC and maintained at that level for 10 min. Thereafter, it was decreased to 0.5 MAC for 10 min. Blood pressure, heart rate, and plasma concentrations of epinephrine and norepinephrine were measured.Results The blood pressure decreased significantly in both groups after increasing the anesthetic concentration, and it increased after decreasing the concentration. The decrease in systolic blood pressure was significantly larger in the isoflurane group. The heart rate increased significantly after increasing the anesthetic concentration only in the isoflurane group. Plasma concentrations of epinephrine and norepinephrine increased significantly in the isoflurane group, whereas the epinephrine concentration (but not the norepinephrine concentration) decreased in the sevoflurane group.Conclusion During surgery a sudden increase in isoflurane concentration induced larger changes in hemodynamics and sympathetic nerve activity than sevoflurane.     

The effects of isoflurane and isoflurane-nitrous oxide anesthesia on brainstem auditory evoked potentials in humans

Monitoring of brainstem auditory evoked potentials (BAEP) during neurological surgery can provide useful information. However, in order to interpret intraoperative BAEP changes, it is necessary to delineate the influence of anesthesia, including inhalation agents. In this study, we examined the influence of isoflurane and isoflurane-nitrous oxide anesthesia on BAEP in ten healthy volunteers during normothermic, normocapnic, and normotensive conditions. Isoflurane significantly increased the latencies of peaks III, IV, and V at all end-tidal concentrations studied (1.0%, 1.5%, and 2.0%). Addition of 50% nitrous oxide did not influence these findings. The increase in latencies with isoflurane anesthesia, however, was nonlinear and appeared to plateau after 1.5%. We suggest that during isoflurane anesthesia, an intraoperative increase in peak V latency beyond 1.0 msec is best explained by factors other than direct effects of isoflurane.     

Effects of surgical intervention on plasma levels of antidiuretic hormone and alpha-human atrial natriuretic polypeptide under sevoflurane anesthesia

Effects of surgical intervention on plasma levels of antidiuretic hormone (ADH) and alpha-human atrial natriuretic polypeptide (alpha-hANP) under sevoflurane-nitrous oxide-oxygen anesthesia were evaluated in 24 patients, ranged in ages from 15 to 65, who underwent non-abdominal surgery (orthopedic surgery) or abdominal surgery (gastrointestinal or gynecological surgery). Anesthesia was induced and maintained with sevoflurane, nitrous oxide and oxygen. Succinylcholine was administered to facilitate tracheal intubation and pancuronium was given during abdominal surgery when needed. Lactated Ringer's solution was administered intravenously throughout the procedures. Neither plasma ADH nor alpha-hANP levels changed significantly during sevoflurane anesthesia alone for 20 min. Plasma ADH levels were unchanged during surgery in patients who underwent non-abdominal surgery, but they tended to increase although insignificantly after the recovery from anesthesia. On the contrary, plasma ADH levels increased significantly during surgery and in the recovery room in patients who underwent abdominal surgery. Plasma alpha-hANP levels were unchanged during surgery and in the recovery room in patients who underwent non-abdominal or abdominal surgery. The authors' findings suggest that ADH secretion was significantly stimulated with abdominal intervention but not with orthopedic one, furthermore neither anesthesia nor surgical stress induced any influence on plasma alpha-hANP levels.     

Effects of sevoflurane anesthesia and surgery on plasma catecholamine levels

Effects of sevoflurane-nitrous oxide-oxygen anesthesia and surgery on plasma levels of epinephrine, norepinephrine and dopamine were evaluated in twenty four patients who ranged in ages from 15 to 65 years. They underwent non-abdominal surgery (orthopedic surgery) or abdominal surgery (gastrointestinal or gynecological surgery). Anesthesia was induced and maintained with sevoflurane in 50% nitrous oxide and 50% oxygen. Succinylcholine was administered intravenously to facilitate tracheal intubation and pancuronium was given intravenously during surgery. Lactated Ringer's solution at a speed of 5-15 ml.kg-1.h-1 was also administered intravenously throughout the procedures. Neither plasma epinephrine, norepinephrine nor dopamine levels changed significantly during the anesthetic induction with sevoflurane anesthesia. Plasma catecholamines were unchanged during and after surgery in patients who underwent non-abdominal surgery, while plasma epinephrine and norepinephrine levels increased significantly during and after abdominal surgery. Plasma dopamine levels, however, were unchanged during and after surgery in these patients. The findings suggest that epinephrine and norepinephrine secretion was significantly stimulated with abdominal intervention but not with orthopedic one under sevoflurane anesthesia.     

Nicardipine did not activate renin-angiotensin-aldosterone system during isoflurane or sevoflurane anesthesia

PURPOSE: To investigate the changes of renin-angiotensin-aldosterone system by nicardipine administration during isoflurane or sevoflurane anesthesia. METHODS: Twenty patients aged 40 to 70 yr for elective neurosurgery were studied. Anesthesia was induced with thiopental, midazolam and fentanyl and was maintained with nitrous oxide in oxygen and isoflurane or sevoflurane. When blood pressure was constant, 0.017 mg x kg(-1) nicardipine was administered as a bolus. Blood pressure, heart rate, and plasma concentrations of nicardipine, angiotensin I and II, aldosterone and renin activity were measured for 30 min after nicardipine administration. RESULTS: Blood pressure decreased for 30 min after nicardipine administration in both groups with lower values during sevoflurane anesthesia. Heart rate increased only in the isoflurane group. Plasma nicardipine concentrations did not differ between isoflurane and sevoflurane groups. Plasma renin activity and concentrations of angiotensin II and aldosterone did not change in either groups and there were no differences between groups. Plasma concentration of angiotensin I increased at 20 and 30 min after nicardipine administration in the isoflurane group but not in the sevoflurane group. CONCLUSION: The activity of renin-angiotensin-aldosterone system did not increase by a single dose administration of nicardipine in isoflurane or sevoflurane anesthesia.     

A comparison of liver function after hepatectomy in cirrhotic patients between sevoflurane and isoflurane in anesthesia with nitrous oxide and epidural block

In this study, we compared postoperative liver function in patients with liver cirrhosis between isoflurane and sevoflurane anesthesia with nitrous oxide (N(2)O) and epidural block. Forty cirrhotic patients with Child-Pugh Grade A, aged 40 to 70 yr, scheduled for liver segmentectomy, had anesthesia induced with midazolam 0.1 mg/kg and fentanyl 4 micro g/kg. For maintenance, intermittent epidural administration of 1.5% lidocaine 4 to 6 mL and sevoflurane (sevoflurane group) or isoflurane (isoflurane group) with N(2)O 3 L/min in oxygen 3 L/min was used. Aspartate aminotransferase, alanine aminotransferase, total bilirubin, alkaline phosphatase, choline esterase, albumin, prothrombin time, and platelet count were measured before and 1, 3, and 7 days after surgery. Aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase increased significantly, with the peaks at 3 days after surgery in both groups. The increases in these variables were significantly larger in the isoflurane group than those in the sevoflurane group. No patient developed hepatic failure. All increases in liver enzymes were small and of questionable clinical relevance. Whether sevoflurane might be a better anesthetic when combined with N(2)O and epidural block for cirrhotic patients than isoflurane with respect to liver damage remains to be determined. IMPLICATIONS: In cirrhotic patients with Child-Pugh Grade A, isoflurane induced more of an increase in serum concentrations of liver enzymes after surgery than sevoflurane when combined with nitrous oxide and epidural block. However, the increases were small, and there was no clinical liver damage.     

A comparison: The efficacy of sevoflurane-nitrous oxide or propofol-nitrous oxide for the induction and maintenance of general anesthesia

Study Objective: To compare sevoflurane-nitrous oxide with propofol-nitrous oxide for the induction and maintenance of anesthesia, and to determine the rates of recovery following each anesthetic.Design: Randomized, controlled study.Setting: Teaching hospital.Patients: 50 ASA physical status I and II patients, ranging in age from 18 to 70 years.Interventions: General anesthesia was induced with either sevoflurane or propofol and maintained with 60 % to 70% nitrous oxide and either sevoflurane or a propofol infusion and supplemental fentanyl. At the conclusion of surgery, the oxygen flow was increased to 6 L/min and all anesthetics were discontinued simultaneously. Patients were monitored for the nature and speed of induction and emergency from anesthesia.Measurements and Main Results: Induction of anesthesia was significantly slower in the sevoflurane group than in the propofol group (2.0 ± 1.1 vs. 0.8 ± 0.5 min, respectively). The ease of induction and the time required for emergence from anesthesia were the same in both study groups (eye opening: 9.0 ± 4.4 min vs. 8.0 ± 5.0 min; following commands: 11.2 ± 5.0 min vs. 9.8 ± 6.9 min; extubation: 9.1 ± 4.5 min vs. 8.6 vs. 5.1 min in the sevoflurane and propofol groups, respectively). Patients in the sevoflurane group experienced nausea and vomiting more frequently than patients in the propofol group (13 and 5 patients vs. 3 and 0 patients in the sevoflurane and propofol groups, respectively), which were not related to the administration of neostigmine or intraoperative opioids.Conclusion: Sevoflurane allows for rapid inhalation induction of, and emergence from, general anesthesia.     

Treatment of stress response during balanced anesthesia. Comparative effects of isoflurane, alfentanil, and trimethaphan.

Acute hypertensive responses during nitrous oxide-opioid-relaxant anesthesia are a common clinical problem. In adult men undergoing radical prostatectomy procedures and anesthetized with a standardized technique, we evaluated the effectiveness of alfentanil, isoflurane, and trimethaphan in treating acute hemodynamic and stress hormone responses to surgical stimulation. Stress hormone concentrations were measured 1 min before skin incision, after the onset of an acute hypertensive response, and after returning the mean arterial pressure to within 10% of the preincision values with one of the three treatment modalities. Pretreatment plasma alfentanil concentrations (151 +/- 47 to 156 +/- 47 ng.ml-1) and end-tidal nitrous oxide concentrations (66 +/- 2 to 68 +/- 2%) were similar in all three groups. Acute hypertensive events were associated with significantly increased concentrations of catecholamines and vasopressin (antidiuretic hormone [ADH]). Whereas intravenous alfentanil returned all hormone concentrations to preincision values, norepinephrine and glucose concentrations were significantly increased after adjunctive isoflurane administration. Although trimethaphan decreased the norepinephrine concentration, the epinephrine, beta-endorphin, cortisol, ADH, and glucose concentrations were significantly increased compared to preincision values. However, the persistent elevation in the posttreatment ADH concentration in the trimethaphan group was the only significant difference between the three groups. Mean (+/- standard deviation) times to awakening (2.8 +/- 3.3 to 3.8 +/- 4.2 min), extubation (8.1 +/- 4.8 to 10.3 +/- 8.5 min), and orientation (19.6 +/- 20.4 to 24.6 +/- 19.1 min) were similar in all three groups. Naloxone was required more frequently in patients in the alfentanil (35%) and isoflurane (24%) groups than in the trimethaphan group (4%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Glucose homeostasis and insulin secretion during isoflurane anesthesia in humans

The effect of isoflurane-air anesthesia on glucose tolerance in humans was investigated using two successive intravenous glucose tolerance tests (IVGTT). After a first IVGTT while awake, patients received a second IVGTT either while awake (group I), during anesthesia with isoflurane-air and pancuronium without surgical stimulation (group II), or during the same anesthetic technique but combined with surgery (group III). Isoflurane seemed to induce glucose intolerance (glucose disappearance rate K10-60 min = 1.628 +/- 0.462% min-1 [control] versus 1.086 +/- 0.920% min-1 [anesthesia], P less than 0.05) partly due to a decreased glucose induced insulin response. Growth hormone and norepinephrine levels were also increased during anesthesia. Epinephrine levels were lowered by isoflurane anesthesia. Although glucose intolerance was marked during surgery (K10-60 min = 0.892 +/- 0.286% min-1), the glucose-induced insulin response remained similar to that observed in patients in group II, while growth hormone, cortisol, epinephrine, and norepinephrine concentrations increased significantly. These known stress factors thus seemed to enhance glucose intolerance through a diminished response to insulin action and/or an enhanced hepatic glucose output, rather than by further impairing pancreatic insulin secretion.     

Perioperative stress response in elderly patients for elective gastrectomy--the comparison between isoflurane anesthesia and sevoflurane anesthesia both combined with epidural anesthesia

The difference in stress responses between isoflurane anesthesia (I group) and sevoflurane anesthesia (S group) was studied. Twelve patients for elective gastrectomy were divided into two groups: S group, 7 patients, 78 +/- 4.3 years of age, and I group, 5 patients, 77.4 +/- 6.9 years of age. Anesthesia was induced by fentanyl, midazolam and sevoflurane or isoflurane with 100% oxygen. After laryngeal mask air way was inserted under spontaneous ventilation, anesthesia was maintained with air (3 l.min-1), oxygen (2 l.min-1), sevoflurane or isoflurane and epidural block. Vecuronium bromide was given during surgery when needed. The demographic data were not different between the two groups. During operation, it was confirmed that the responses of sympathetic nervous system (epinephrine, norepinephrine) and pituitary-adrenocortical system (ACTH, cortisol) were maintained in both groups. After operation plasma norepinephrine levels increased in both groups. Although the responses of I group tended to be stronger than that of S group, there was no significant difference between the two groups.     

Clinical comparison of sevoflurane and isoflurane when administered with nitrous oxide for surgical procedures of intermediate duration

The purpose of this study was to compare the haemodynamic effects and emergence times of anaesthesia with sevoflurane with those of isoflurane when the agents were administered with nitrous oxide to adult inpatients (ASA I and II) undergoing surgery of at least an hour in duration. Fifty patients were randomly assigned to receive either 0.65 minimum alveolar concentration (MAC) (1.3%) sevoflurane or 0.65 MAC (0.8%) isoflurane together with 60% nitrous oxide following induction with thiopentone, fentanyl, and succinylcholine. Systemic blood pressure and heart rate trends were similar for both groups for the duration of anaesthesia. However, differences in systolic blood pressure measurements were noted at one minute after incision (99 ± 3 mmHg, mean ± SE, in the sevoflurane group compared with 109 ± 4 mmHg for isoflurane), and at emergence (125 ± 3 mmHg for sevoflurane, 134 ± 3 mmHg for isoflurane), and in diastolic blood pressure measurements at five minutes after intubation (64 ± 2 mmHg for sevoflurane, 73 ± 3 mmHg for isoflurane). Recovery of response to command was more rapid after discontinuation of sevofluranenitrous oxide (9.9 ± 1.1 min) than after isoflurane-nitrous oxide (13.9 ± 1.3 min). Despite earlier emergence, patients who had received sevoflurane did not request postoperative analgesia sooner. We conclude that the purported advantages of sevoflurane, namely haemodynamic stability and rapid emergence, can be expected even when the agent is administered at 0.65 MAC (1.3%) in nitrous oxide to a typical adult surgical population undergoing procedures of intermediate duration (2.3 ± 0.2 hr).     

The stress reaction in the recovery phase from halothane and isoflurane anesthesia

This study was undertaken to investigate the influences of halothane and isoflurane as well as different extubation techniques on the endocrine stress response during recovery from general anesthesia. Forty patients scheduled for herniorrhaphy and cholecystectomy were randomly allocated to 4 groups: 20 received halothane and 20 received isoflurane anesthesia. Within the halothane and isoflurane groups, 10 patients each were extubated during anesthesia (1/2 MAC) and a further 10 had awake extubation. Premedication, induction of anesthesia, and intraoperative anesthetic management were standardized in all groups. Plasma levels of endocrine stress parameters as well as mean arterial pressure (MAP), heart rate (HR), and arterial oxygen saturation (SaO2) were measured at nine time points up to 60 min after extubation. Biometric data and duration of operation and anesthesia were comparable in all groups. In the recovery period, epinephrine levels were higher in the isoflurane groups than in the halothane groups (P = 0.02). With respect to time course, earlier and more marked increases of epinephrine, norepinephrine, and antidiuretic hormone (ADH) levels were observed in the isoflurane groups compared to the halothane groups (P less than 0.01), representing the more rapid elimination of isoflurane. The sympathoadrenergic stress response was more pronounced in patients with extubation during anesthesia than in those with awake extubation: epinephrine levels were slightly higher and group levels of norepinephrine were significantly increased (P = 0.02). No influence of the extubation techniques was observed on ADH, ACTH, and cortisol levels or on MAP, HR, or SaO2. In summary, extubation during anesthesia did not reduce the endocrine stress response. It is concluded that awake extubation should be preferred unless the operation or the patient's condition requires extubation during anesthesia.     

Randomized controlled trial of total intravenous anesthesia with propofol versus inhalation anesthesia with isoflurane-nitrous oxide: postoperative nausea with vomiting and economic analysis

BACKGROUND: To assess the incidence of postoperative nausea and vomiting after total intravenous anesthesia (TIVA) with propofol versus inhalational anesthesia with isoflurane-nitrous oxide, the authors performed a randomized trial in 2,010 unselected surgical patients in a Dutch academic institution. An economic evaluation was also performed. METHODS: Elective inpatients (1,447) and outpatients (563) were randomly assigned to inhalational anesthesia with isoflurane-nitrous oxide or TIVA with propofol-air. Cumulative incidence of postoperative nausea and vomiting was recorded for 72 h by blinded observers. Cost data of anesthetics, antiemetics, disposables, and equipment were collected. Cost differences caused by duration of postanesthesia care unit stay and hospitalization were analyzed. RESULTS: Total intravenous anesthesia reduced the absolute risk of postoperative nausea and vomiting up to 72 h by 15% among inpatients (from 61% to 46%, P < 0.001) and by 18% among outpatients (from 46% to 28%, P < 0.001). This effect was most pronounced in the early postoperative period. The cost of anesthesia was more than three times greater for propofol TIVA. Median duration of stay in the postanesthesia care unit was 135 min after isoflurane versus 115 min after TIVA for inpatients (P < 0.001) and 160 min after isoflurane versus 150 min after TIVA for outpatients (P = 0.039). Duration of hospitalization was equal in both arms. CONCLUSION: Propofol TIVA results in a clinically relevant reduction of postoperative nausea and vomiting compared with isoflurane-nitrous oxide anesthesia (number needed to treat = 6). Both anesthetic techniques were otherwise similar. Anesthesia costs were more than three times greater for propofol TIVA, without economic gains from shorter stay in the postanesthesia care unit     

七氟醚吸入麻醉与丙泊酚复合七氟醚麻醉对血糖的影响

目的 探讨七氟醚吸入麻醉对血糖水平的影响.方法 30例全麻患者随机分成七氟醚吸人麻醉组(A组)和丙泊酚复合七氟醚麻醉组(B组),每组15例.观察术前以及手术2h时的血糖浓度.结果 A、B两组手术2h的血糖均比术前明显升高[(6.23±1.45)mmol/L vs.(4.86±0.85)mmol/L和(6.66±1.48)mmol/L vs.(5.11±0.43)mmol/L](P<0.05);但组间差异无统计学意义.结论 七氟醚吸人麻醉与内泊酚复合七氟醚麻醉均不能抑制应激性血糖升高.     

BIS值监测患儿七氟醚复合氧化亚氮麻醉深度的准确性

目的 评价BIS值监测患儿七氟醚复合氧化亚氮(N2O)麻醉深度的准确性.方法 择期拟在全麻下行腹部手术患儿72例,年龄1～14岁,ASA分级Ⅰ或Ⅱ级,按年龄分层后随机分为3组(n=24):七氟醚组(S组)、七氟醚+30% N2O组(SN1组)和七氟醚+60% N2O组(SN2组).静脉注射阿托品、利多卡因、异丙酚、罗库溴铵和瑞芬太尼麻醉诱导,气管插管后行机械通气,维持PET CO2 35～45 mm Hg;吸入2.5%七氟醚维持麻醉,SN1组和SN2组分别复合吸入30%和60%N2O.手术开始时调节七氟醚吸入浓度,使七氟醚呼气末浓度(CETSev)分别达到2.5%、2.0%和1.5%,每个CETSev维持10 min视为稳态;此后调节七氟醚吸入浓度,维持BIS值40～60.于麻醉诱导前和CETSev达稳态时记录BIS值;于BIS值40～60维持20 min时记录CETSev(C50).结果 与S组比较,SN1组BIS值和C50差异无统计学意义(P＞0.05);与S组及SN1组比较,SN2组BIS值和C50降低(P＜0.05);S组、SN1组和SN2组BIS值与CETSev间的相关系数分别为-0.736、-0.817和-0.729(P＜0.01),三组相关系数比较差异无统计学意义(P＞0.05).结论 BIS值可准确地监测患儿吸人七氟醚复合N2O时的麻醉深度.     

Nitrous oxide induces paradoxical electroencephalographic changes after tracheal intubation during isoflurane and sevoflurane anesthesia

In this randomized, double-blind, controlled study, we tested the hypothesis that nitrous oxide (N2O) affects bispectral index (BIS) and 95% spectral edge frequency (SEF95) in response to tracheal intubation during anesthesia with isoflurane and sevoflurane. In protocol 1, we randomly allocated 90 ASA physical status I patients to 6 groups (n = 15 each). Anesthesia was induced with isoflurane or sevoflurane with 0%, 33%, or 66% N2O. The concentration of isoflurane and sevoflurane was gradually increased and end-tidal concentrations were maintained at 1.1% and 1.7%, respectively. Tracheal intubation was performed 12 min after induction of anesthesia. BIS was significantly increased 1 min after tracheal intubation compared before laryngoscopy in patients receiving only isoflurane or sevoflurane (P = 0.001 and 0.007, respectively). In patients receiving 66% N2O-isoflurane or 66% N2O-sevoflurane, both BIS and SEF95 were significantly decreased after tracheal intubation and significantly lower than in those patients receiving only isoflurane or sevoflurane, respectively (P < 0.01 for both). In protocol 2, 3 microg/kg of IV fentanyl completely abolished the decrease of BIS and SEF95 after tracheal intubation during anesthesia with 66% N2O-isoflurane and 66% N2O-sevoflurane (n = 10). We conclude that 66% N2O induced a paradoxical decrease of BIS in response to tracheal intubation during anesthesia with isoflurane and sevoflurane.     

Recovery and pharmacokinetic parameters of desflurane, sevoflurane, and isoflurane in patients undergoing urologic procedures.

STUDY OBJECTIVE: To compare the pharmacokinetics and the speed of recovery after inhalation anesthesia with desflurane, sevoflurane, and isoflurane in elective surgery. DESIGN: Prospective, randomized study. SETTING: University medical center. PATIENTS: 30 ASA physical status I and II adults presenting for elective surgery. INTERVENTIONS: Anesthesia was induced with etomidate and maintained with desflurane (n = 10), sevoflurane (n = 10), or isoflurane (n = 10) and nitrous oxide. The inhalation drugs were titrated until an adequate clinical depth of anesthesia was reached. At the end of anesthesia, the patients breathed oxygen via the endotracheal tube and after extubation via a face mask. MEASUREMENTS AND MAIN RESULTS: The groups were similar with respect to age, weight, duration of anesthesia, and mean arterial pressure. Mean end-tidal concentration (FA = FA0) at the end of anesthesia was 6.34 +/- 1.15% after desflurane, 1.85 +/- 0.42% after sevoflurane, and 1.10 +/- 0.24% after isoflurane. FA/FA0 decreased significantly faster with desflurane than with isoflurane, while there was little difference between desflurane and sevoflurane. As for the terminal half-life (t1/2), there were no differences among the groups (8.16 +/- 3.15 min after desflurane, 9.47 +/- 4.46 min after sevoflurane, and 10.0 +/- 5.57 min after isoflurane). The time until a command was followed for the first time was the same in all three groups (13.0 +/- 4.7 min after desflurane, 13.4 +/- 4.4 min after sevoflurane, and 13.6 +/- 3.4 min after isoflurane). There was no significant correlation between duration of anesthesia and the time until recovery. CONCLUSIONS: There are only minor differences with regard to the recovery phase in premedicated patients who receive clinically titrated inhalation anesthesia with desflurane, sevoflurane, or isoflurane.     

Plasma inorganic fluoride with sevoflurane anesthesia: correlation with indices of hepatic and renal function.

The biotransformation and plasma inorganic fluoride ion production of sevoflurane (the new volatile anesthetic) during and after surgical anesthesia was studied in 50 ASA I or II surgical patients. Twenty-five additional patients served as controls by receiving isoflurane. Sevoflurane or isoflurane was administered with a semiclosed (total gas flow, 2 L/min O2) circle absorption system for durations of 1.0 to greater than 7.0 minimal alveolar concentration (MAC) hours for surgical anesthesia (sevoflurane MAC, 2.05%; isoflurane MAC, 1.15%). Preoperative and postoperative blood urea nitrogen and creatinine concentrations were determined. Blood samples were obtained during and after anesthesia in both groups for determining anesthetic blood concentration analysis and plasma fluoride level. Plasma fluoride concentrations did not significantly increase during isoflurane anesthesia. Sevoflurane biotransformation produced a mean peak plasma inorganic fluoride concentration of 29.3 +/- 1.8 mumol/L, 2 h after anesthesia, which decreased to 18 mumol/L concentration by 8 h after anesthesia. The peak plasma inorganic fluoride ion concentration correlated with duration of sevoflurane anesthetic exposure. Five patients given sevoflurane had peak levels transiently exceeding 50 mumol/L, and one of these had a history of ingesting drugs potentially producing hepatic enzyme induction. No increases in postoperative levels of creatinine, blood urea nitrogen, direct bilirubin, or hepatic transaminase and no changes in serum electrolyte level occurred in either anesthetic group. Indirect bilirubin concentration increased significantly after sevoflurane anesthesia, but the increase was not of clinical significance (from 0.30 +/- 0.03 to 0.38 +/- 0.06 mg/dL). Indirect bilirubin concentrations did not increase after isoflurane anesthesia; the concentrations reached 0.31 +/- 0.04 mg/dL and did not differ significantly from those found with sevoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)