Fentanyl Augments the Blockade of the Sympathetic Response to Incision (MAC-BAR) Produced by Desflurane and Isoflurane: Desflurane and Isoflurane MAC-BAR without and with Fentanyl

Background: Heart rate (HR) or mean arterial blood pressure (MAP) may increase in response to incision despite the absence of a motor response. The authors hypothesized that the MAC-BAR (minimum alveolar concentration of an anesthetic that blocks adrenergic response to incision) for isoflurane would exceed that for desflurane, and that fentanyl would decrease the MAC-BAR for each anesthetic in a dose-dependent manner.

Methods: Seventy-one patients were randomly allocated to one of six groups: desflurane or isoflurane without fentanyl or with 1.5 or 3 micro gram/kg fentanyl given intravenously 5 min before surgical incision. Anesthesia was induced with 2 mg/kg propofol given intravenously, and tracheal intubation facilitated with 0.1 mg/kg given intravenously. The first patient in each group received 1 MAC (end-tidal) of the inhaled anesthetic in 60% nitrous oxide (0.55 MAC), balance oxygen, maintained for at least 10 min before incision. The response was considered positive if the HR or MAP increased 15% or more. If the response was positive, the end-tidal concentration given to the next patient was 0.3 MAC greater; if the response was negative, the end-tidal concentration was 0.3 MAC less. The MAC-BAR level was calculated as the mean of four independent cross-over responses in each group.

Results: Desflurane and isoflurane anesthesia with 60% nitrous oxide did not change HR (P > 0.05) and decreased MAP (P < 0.05) before incision. Plasma epinephrine and norepinephrine concentrations after anesthesia and before incision were normal in all groups. The MAC-BAR level, without fentanyl, did not differ (P > 0.05) between desflurane (1.30 +/- 0.34 MAC [mean +/- SD]) and isoflurane (1.30 +/- 0.18 MAC). Fentanyl given at 1.5 micro gram/kg intravenously equivalently (P > 0.05) reduced the MAC-BAR for desflurane (to 0.40 +/- 0.18 MAC; P <0.05) and isoflurane (to 0.55 +/- 0.00 MAC; P < 0.05), but a further increase in fentanyl to 3 micro gram/kg caused no greater decrease in the MAC-BAR for desflurane (0.48 +/- 0.16 MAC) and isoflurane (0.40 +/- 0.30 MAC).     

MAC of desflurane in 60% nitrous oxide in infants and children.

Desflurane, an inhaled anesthetic, may be useful for outpatient procedures in pediatric patients because its blood solubility (similar to that of nitrous oxide and less than that of commercially available potent inhaled anesthetics) may facilitate emergence and recovery from anesthesia. Although the MAC of desflurane without nitrous oxide has been determined in pediatric patients, it is likely that clinicians will administer desflurane with nitrous oxide. To determine the potency of desflurane administered with 60% nitrous oxide in pediatric patients, the authors determined the minimum alveolar concentration that prevents movement in 50% of subjects (MAC) in 12 infants aged 17 weeks-12 months and 12 children aged 1-5 yr. Anesthesia was induced with desflurane in oxygen; nitrous oxide was not administered during induction of anesthesia to minimize the likelihood of hypoxia if laryngospasm occurred. Following tracheal intubation, nitrous oxide and desflurane were administered and maintained at target concentrations for a minimum of 10 min before surgical incision. No additional anesthetic, sedative/hypnotic, or analgesic drugs were administered prior to incision. Following surgical incision, anesthesia was maintained with nitrous oxide, desflurane, and fentanyl, 4 +/- 1 micrograms/kg (mean +/- SD). MAC, determined using a modification of Dixon's "up-and-down" technique, was 7.5 +/- 0.1% (mean +/- SE) for infants and 6.4 +/- 0.2% for children; similar values were obtained using logistic regression (7.5 +/- 0.01% and 6.3 +/- 0.03%, respectively). Time from discontinuation of anesthesia to eye-opening and tracheal extubation was 5.4 +/- 3.6 min (mean +/- SD).(ABSTRACT TRUNCATED AT 250 WORDS)     

Percutaneous recording of muscle nerve sympathetic activity during propofol, nitrous oxide, and isoflurane anesthesia in humans

The effects of propofol, nitrous oxide, and/or isoflurane on efferent activity of sympathetic muscle nerve fibers (MSA) were studied using percutaneous microneurographic recordings from the peroneal nerve. Eight ASA Physical Status 1 patients (30-70 yr of age) scheduled for otorhinolaryngeal surgery entered the study. The effects of propofol (2-2.5 mg.kg-1.min-1) induction, tracheal intubation, and maintenance of anesthesia with isoflurane (0.3%, 0.6%, and 1.2% end-tidal concentrations) and/or 70% nitrous oxide were studied with respect to MSA, arterial blood pressure, heart rate, and indices of skin blood flow (laser doppler photometry and finger pulse plethysmography). Induction of anesthesia with propofol decreased MSA to 34 +/- 2% (mean +/- SEM) (P less than 0.05), and subsequent tracheal intubation increased MSA rapidly to 151 +/- 23% (P less than 0.05) of the control level. Isoflurane administration both with and without nitrous oxide led to a decrease of MSA (P less than 0.05). However, during nitrous oxide/isoflurane anesthesia (1.0 MAC) MSA was 76 +/- 38% higher than when isoflurane was used alone, although this implied a decrease in anesthetic depth to 0.5 MAC. This indicates that nitrous oxide and isoflurane have opposite effects on sympathetic outflow. During undisturbed propofol, nitrous oxide, and/or isoflurane administration (up to 1.0 MAC), MSA retained its normal pulse synchronous pattern, indicating that modulation of sympathetic outflow from arterial baroreceptors was still present. Skin blood flow increased sevenfold to tenfold in association with propofol induction (P less than 0.05) and was maintained at an 11- to 19-fold increase during nitrous oxide and/or isoflurane anesthesia, without any difference between the two anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)     

The relationship between end-tidal isoflurane concentration and electroencephalographic bispectral index during isoflurane/epidural anesthesia

We studied the effects of increases in isoflurane concentration on the bispectral index (BIS) in 16 patients undergoing lower abdominal surgery during isoflurane/epidural anesthesia. In 8 patients, the lungs were ventilated with an air/oxygen mixture (inspired oxygen fraction 0.33) [N(-) group], and in another 8 patients, the lungs were ventilated with 66% nitrous oxide in oxygen [N(+) group]. During surgery, patients received 1.0 MAC (1.15%) end-tidal isoflurane and the BIS was recorded after 10 min of unchanged end-tidal concentration. After this, we increased the end-tidal concentration of isoflurane by 0.2 MAC to 1.8 MAC. At each concentration step, the BIS was recorded again after 10 min of unchanged end-tidal concentration. At isoflurane concentration < 1.4 MAC, the BIS did not change with increasing isoflurane concentration in both groups (BIS values = about 40). In N (-) group, the BIS decreased in all patients at isoflurane concentration > 1.6 MAC. The mean BIS values were 22 (SD 18) at 1.6 MAC and 2(4) at 1.8 MAC, respectively. In N (+) group, the BIS decreased in four patients at isoflurane concentration > 1.6 MAC, and the BIS did not decrease at 1.8 MAC in another four patients. The mean BIS values were 27 (17) at 1.6 MAC and 21(21) at 1.8 MAC. The present data suggest that BIS may not correlate with anesthetic effect of isoflurane at isoflurane concentration > 1.0 MAC.     

The epileptogenic properties of the volatile anesthetics sevoflurane and isoflurane in patients with epilepsy

No study comparing epileptogenicity of sevoflurane to other volatile anesthetics has been performed. We compared the epileptogenic properties of sevoflurane to isoflurane in patients with epilepsy. In 24 mentally and/or physically disabled patients, 12 with epilepsy and 12 without epilepsy, electroencephalograms were recorded under anesthesia with 1.0 minimum alveolar anesthetic concentration (MAC), 1.5 MAC, and then 2.0 MAC sevoflurane or isoflurane under three ventilatory conditions: (A) 100% oxygen, and end-tidal CO(2) partial pressure (ETCO(2)) = 40 mm Hg, (B) 50% oxygen, 50% nitrous oxide, ETCO(2) = 40 mm Hg, and (C) 100% oxygen, ETCO(2) = 20 mm Hg. Spike activity was evaluated as a spike-and-wave index (% durations of spike and wave). The spike-and-wave index increased (P<0.05) from 1.99%+/-0.96% during 1.0 MAC sevoflurane to 6.14% +/- 4.45% during 2.0 MAC sevoflurane in (A) in the epilepsy group, while no spike activity was observed in the nonepilepsy group. Only a few spikes were observed under isoflurane anesthesia, 0.04% +/- 0.04% in (A), with no spikes in (B) and (C). Supplementation with 50% nitrous oxide or hyperventilation (P<0.05) suppressed the occurrence of spikes. Sevoflurane has a stronger epileptogenic property than isoflurane, but nitrous oxide or hyperventilation counteracts this specific epileptogenic property. Implications: The stronger epileptogenicity of sevoflurane than isoflurane was confirmed in a controlled study in patients with epilepsy. Hyperventilation and supplementation of nitrous oxide under sevoflurane anesthesia suppressed epileptogenicity. A combination of sevoflurane and nitrous oxide may be a safer method for seizure-prone patients than the use of sevoflurane alone.     

Low flow anesthesia at a fresh gas flow of 10 ml.kg-1.min-1 for hours using time-cycled ventilator]

Low flow anesthesia (LFA) at a fresh gas flow (FGF) level of 10 ml.kg-1.min-1 with oxygen flow set at 0.5 ml.kg-1.min-1: 0.5 ml.kg-1.min-1 nitrous oxide and 3% isoflurane was performed using time-cycled ventilator on 10 patients of ASA class I or II, with age of 55 +/- 13 (mean +/- SD) years and body weight of 55 +/- 10 kg for 5 h. Excessive anesthetic gases from the anesthesia gas monitor were led to an expiratory breathing tube. After rapid induction and tracheal intubation, denitrogenation was performed for about 5 min using a 100% oxygen flow of 6 l.min-1 before LFA. The inspired/expired oxygen concentration decreased gradually from 96 +/- 2%/90 +/- 2% at beginning of LFA to 42 +/- 3%/37 +/- 4% at 5 h. The operation was started after 29 +/- 10 min of beginning of LFA. The nitrous oxide concentration reached 37 +/- 4%/35 +/- 4% at the beginning of operation and further increased to 55 +/- 3%/53 +/- 3% at 5 h. The isoflurane concentration reached 1.0 +/- 0.1%/0.8 +/- 0.1% at the beginning of operation and further increased to 1.2 +/- 0.1%/1.0 +/- 0.1% at 5 h. The anesthetic potency was 1.2 +/- 0.1 MAC/1.0 +/- 0.2 MAC at the beginning of operation. The isoflurane vaporizer setting was changed only once in two cases from 3% to 2% exceeding 1.5% in inspired concentration. There was no need to change the flow of oxygen and nitrous oxide for 5 hrs. No SpO2 lower than 95% was observed during this study. This method is a clinically safe, easily applicable anesthesia method and used the smallest FGF reported in LFA without occurrence of low FIO2.     

Plasma lidocaine concentrations during epidural blockade with isoflurane or halothane anesthesia.

Because isoflurane maintains hepatic blood flow at higher flows than halothane, we proposed that the elimination of lidocaine would be different between these two volatile anesthetics. The plasma lidocaine concentrations were determined in 14 female patients undergoing epidural blockade plus isoflurane anesthesia and compared with those obtained during halothane anesthesia for lower abdominal surgery. General anesthesia was maintained with isoflurane (0.46% +/- 0.04% [mean +/- SE] inspired, n = 7) or halothane (0.48% +/- 0.05% inspired, n = 7) and 67% nitrous oxide in oxygen. All patients received 2% lidocaine solution, 10 mL as a bolus dose and continuous administration at a rate of 10 mL/h, through the epidural catheter. The plasma lidocaine concentrations over 180 min after the epidural injection in patients receiving isoflurane were similar to those in patients receiving halothane. The results suggest that low inspired concentrations of isoflurane do not reduce plasma lidocaine concentrations in patients during epidural blockade, compared with halothane.     

Sevoflurane speeds recovery of baroreflex control of heart rate after minor surgical procedures compared with isoflurane.

Volatile anesthetics attenuate arterial baroreflex functions, whereas noxious stimuli may modify baroreflex-induced circulatory responses during anesthesia. We designed the present study to compare baroreflex control of heart rate during sevoflurane and isoflurane anesthesia in young healthy surgical patients. Baroreflex sensitivity was assessed in 24 patients randomized to receive either sevoflurane (n = 12) or isoflurane (n = 12) for general anesthesia. After an 8- to 10-h fast and no premedication, measurements of RR intervals obtained from electrocardiography and systolic blood pressure (SBP) measured through a radial artery catheter were made at conscious baseline (Awake), during end-tidal sevoflurane 2% or isoflurane 1.2% plus 67% nitrous oxide before incision (Anesth), during surgery at end-tidal sevoflurane 2% or isoflurane 1.2% plus 67% nitrous oxide (Surg), and 20 min after tracheal extubation (Recov). Baroreflex responses were triggered by bolus i.v. injections of phenylephrine (100-150 micrograms) and nitroprusside (100-150 micrograms) to increase and decrease SBP by 15-30 mm Hg, respectively. The linear portions of the baroreflex curves relating RR intervals and SBP were determined to obtain baroreflex sensitivities. Baroreflex sensitivities to both pressor and depressor tests were significantly depressed during Anesth and Surg periods compared with Awake values in both anesthetic techniques. The pressor test sensitivity during the Recov period returned to the Awake value after sevoflurane (12.9 +/- 3.7 vs 11.0 +/- 8.7 ms/mm Hg [mean +/- SD]) but was still depressed after isoflurane anesthesia (13.9 +/- 8.0 vs 4.8 +/- 3.2 ms/mm Hg; P < 0.05). The depressor test sensitivities during the Recov period remained depressed after both anesthetic techniques. We conclude that both sevoflurane and isoflurane depress arterial baroreflex function during anesthesia and surgery, but the pressor test sensitivity was restored more quickly after sevoflurane than after isoflurane anesthesia. Implications: Arterial baroreflex function is an important neural control system for maintaining cardiovascular stability. We found that baroreflex control of heart rate due to hypertensive perturbation returned to the preanesthetic level more quickly after sevoflurane than after isoflurane anesthesia.     

The Effect of Isoflurane, Halothane, Sevoflurane, and Thiopental/Nitrous Oxide on Respiratory System Resistance after Tracheal Intubation

Background: After tracheal intubation, lung resistance and therefore respiratory system resistance (Rrs) routinely increase, sometimes to the point of clinical bronchospasm. Volatile anesthetics generally have been considered to be effective bronchodilators, although there are few human data comparing the efficacy of available agents. This study compared the bronchodilating efficacy of four anesthetic maintenance regimens: 1.1 minimum alveolar concentration (MAC) end-tidal sevoflurane, isoflurane or halothane, and thiopental/nitrous oxide.

Methods: Sixty-six patients underwent tracheal intubation after administration of 2 micro gram/kg fentanyl, 5 mg/kg thiopental, and 1 mg/kg succinylcholine. Vecuronium or pancuronium (0.1 mg/kg) was then given to ensure paralysis during the rest of the study. Postintubation R sub rs was measured using the isovolume technique. Maintenance anesthesia was then randomized to thiopental 0.25 mg [center dot] kg sup -1 [center dot] min sup -1 plus 50% nitrous oxide, or 1.1 MAC end-tidal isoflurane, halothane, or sevoflurane. The Rrs was measured after 5 and 10 min of maintenance anesthesia. Data were expressed as means +/- SD.

Results: Maintenance with thiopental/nitrous oxide failed to decrease Rrs, whereas all three volatile anesthetics significantly decreased Rrs at 5 min with little further improvement at 10 min. Sevoflurane decreased Rrs more than either halothane or isoflurane (P < 0.05; 58 +/- 14% of the postintubation Rrs vs. 69 +/- 20% and 75 +/- 13%, respectively).     

Additive contribution of nitrous oxide to halothane MAC in infants and children

Fifty-one infants and small children (14.7 +/- 7.2 mo) were studied to determine the MAC of halothane in O2 (n = 11) and in the presence of three different nitrous oxide (N2O) concentrations (25% [n = 13], 50% [n = 13], and 75% [n = 14]). In the three N2O groups, after randomly assigning patients to an N2O group, anesthesia was induced with halothane and N2O using a pediatric circle system. After endotracheal intubation, halothane and N2O end-expired concentrations were adjusted to predetermined concentrations. The initial halothane concentrations in each group were based on the assumption that each percent N2O reduced halothane concentrations by 0.01 vol % (assumed halothane MAC = 1.0 vol %). Based on the response of the preceding subject in each group, halothane concentrations were increased or decreased depending on whether the response was to move or not to move, respectively, in response to the surgical incision. The mean duration of constant end-tidal concentrations before skin incision was 10 min. End-tidal gases were sampled and measured from a separate distal sampling port of an endotracheal tube during controlled ventilation (Perkin-Elmer Mass Spectrometer). The MAC value for halothane in O2 was 0.94 +/- 0.08 vol % (mean +/- SD). The MAC values of halothane in the presence of 25%, 50%, and 75% N2O were 0.78 +/- 0.12 vol %, 0.44 +/- 0.10 vol %, and 0.29 +/- 0.06 vol %, respectively. All concentrations of N2O significantly reduced the MAC of halothane. A regression analysis through all four data points yielded a linear relationship (r2 = 0.87) with a predicted MAC for N2O of 105 vol %. Unlike halothane and isoflurane, the predicted MAC of N2O in infants and children is similar to that reported by others in adults. Similar to the results of clinical studies in adults, the contribution of N2O to halothane MAC in children is additive.     

Comparative hemodynamic depression of halothane versus isoflurane in neonates and infants: an echocardiographic study.

The purpose of this study was to measure and compare the relationship of cardiovascular depression and dose during equal potent levels of halothane and isoflurane anesthesia in neonates (n = 19) (16.7 +/- 6.9 days) and infants (n = 54) (6.1 +/- 3.1 mo). Seventy-three children had heart rate, arterial blood pressure, and pulsed Doppler pulmonary blood flow velocity as well as two-dimensional echocardiographic assessments of left ventricular area and length recorded just before anesthesia induction. Anesthesia was induced by inhalation of increasing inspired concentrations of halothane or isoflurane in oxygen using a pediatric circle system and mask. During controlled ventilation, halothane and isoflurane concentrations were adjusted to maintain 1.0 MAC and then 1.5 MAC (corrected for age), and echocardiographic and hemodynamic measurements were repeated. A final cardiovascular measurement was recorded after intravenous administration of 0.02 mg/kg of atropine. All measurements were completed before tracheal intubation and the start of elective surgery. In neonates, 1.0 MAC concentrations of halothane and isoflurane decreased cardiac output (74% +/- 16%), stroke volume (75% +/- 15%), and ejection fraction (76% +/- 15%) similarly from awake levels. Decreases in cardiac output, stroke volume, and ejection fraction with halothane and isoflurane were significantly larger at 1.5 MAC (approximately 35% decreases from awake values) than at 1.0 MAC. Heart rate decreased significantly during 1.5 MAC halothane anesthesia (94% +/- 4%) but remained unchanged during isoflurane anesthesia. In infants, 1.0 MAC halothane and isoflurane decreased cardiac output (83% +/- 12%), stroke volume (78% +/- 12%), and ejection fraction (74% +/- 12%) when compared with awake measures.(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.     

Effect of inspired nitrous oxide concentration on the rate of fall of alveolar concentration: reversed concentration effect

The effect of inspired nitrous oxide concentration on the rate of fall of alveolar nitrous oxide concentration was studied in six patients ranging in age from 25 to 46 years. After equilibrium was reached with nitrous oxide, nitrous oxide administration was stopped and replaced by the same concentration of nitrogen. The decrease in alveolar concentration of nitrous oxide (FE/FE0) was measured continuously, where FE = measured end-tidal concentration of nitrous oxide, and FE0 = the end-tidal concentration immediately preceding the cessation of nitrous oxide administration. The rate of decrease in FE/FE0 was more rapid when 70% nitrous oxide was inspired (Part I) than when 30% nitrous oxide was inspired (Part II). One minute after the cessation of nitrous oxide administration, FE/FE0 was 0.30 +/- 0.03 (mean +/- s.d.) in Part I and 0.36 +/- 0.02 in Part II (P less than 0.05). Mean expired tidal volume increased from 515 +/- 43 ml to 552 +/- 48 ml in Part I and from 510 +/- 48 ml to 526 +/- 39 ml in Part II (P less than 0.05). The authers conclude that the more rapid decrease in alveolar concentration of nitrous oxide (FE/FE0) at higher concentrations of nitrous oxide results from augmentation of expired ventilation. We have called this phenomenon the "reversed concentration effect".     

Relationship between minimum alveolar concentration and electroencephalographic bispectral index as well as spectral edge frequency 95 during isoflurane/epidural or sevoflurane/epidural anesthesia]

To investigate the relationship between minimum alveolar concentration (MAC) and electroencephalographic variables, we measured the bispectral index (BIS) and the spectral edge frequency 95 (SEF 95) in 17 patients undergoing elective surgery during isoflurane/epidural (n = 8) or sevoflurane/epidural (n = 9) anesthesia. Patients received 2.0 MAC end-tidal concentrations of isoflurane or sevoflurane, and the BIS and the SEF 95 were recorded after 15 min of an unchanged end-tidal concentration. The concentration of the inhalational agent was decreased to 1.2 MAC, and measurements were repeated again. During isoflurane anesthesia, the BIS increased significantly (3.6 +/- 3.9 at 2.0 MAC, 43.5 +/- 9.2 at 1.2 MAC [mean +/- SD]). In contrast, the BIS did not change significantly during sevoflurane anesthesia (35.3 +/- 8.4 at 2.0 MAC, 42.8 +/- 6.1 at 1.2 MAC). There were significant differences in the BIS and the SEF 95 at 2.0 MAC between isoflurane and sevoflurane groups. In contrast, the BIS and the SEF 95 showed no difference at 1.2 MAC between the groups. These findings suggest that different inhalational anesthetics may have different effects on the BIS and the SEF 95.     

Induction,maintenance and recovery characteristics of desflurane in infants and children

To determine the induction and recovery characteristics of the new poly-fluorinated anaesthetic desflurane, 78 fasting and unpremedicated neonates, infants and children up to 12 yr of age were studied. Patients were stratified according to age: full-term neonates less than 28 days of age (n = 12), infants 1-6 mth (n = 12) infants 6-12 mth (n = 15), children 1-3 yr (n = 15), 3-5 yr (n = 12), and 5-12 yr (n = 12). After preoxygenation for two minutes and an awake tracheal intubation, neonates were anaesthetized with stepwise increases in the inspired concentration of desflurane in an air/oxygen mixture. Infants 1-12 mth of age and children were anaesthetized with stepwise increases in the inspired concentration of desflurane in oxygen. Their tracheas were intubated under deep desflurane anaesthesia without muscle relaxation. The incidence of airway reflex responses (including breathholding, coughing, laryngospasm, bronchospasm and oropharyngeal secretions), incidence of excitement, minimum arterial oxygen saturation, and times to loss of eyelash reflex and tracheal intubation during induction were recorded. After skin incision, anaesthesia was maintained with desflurane (approximately 1 MAC) in 60% nitrous oxide and oxygen. Heart rate and systolic arterial pressure were recorded awake, at approximately 1 MAC before and after skin incision and throughout surgery. At the completion of surgery, all anaesthetics were discontinued and the lungs were ventilated with 100% oxygen. During emergence, the end-tidal concentration of desflurane was recorded until extubation. The incidence of airway reflex responses and the times to eye opening and extubation after the discontinuation of desflurane were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)     

右美托咪啶对异氟醚抑制切皮时患者体动反应的肺泡气最低有效浓度的影响

目的 探讨右美托咪啶对异氟醚抑制切皮时患者体动反应的肺泡气最低有效浓度(MAC)的影响.方法 择期全身麻醉下行上腹部手术患者,年龄40～60岁,ASA分级Ⅰ或Ⅱ级,体重指数22～27 kg/m2,采用随机数字表法,将患者随机分为3组:对照组(C组)、小剂量右美托咪啶组(D1组)和大剂量右美托咪啶组(D2组).麻醉诱导前静脉输注右美托咪啶(生理盐水稀释至15 ml)0.4 μg/kg(D1组)、0.8μg/kg(D2组)及生理盐水15 ml(C组),15 min内输注完毕.静脉注射芬太尼-异丙酚-琥珀酰胆碱麻醉诱导,气管插管后机械通气并开启异氟醚挥发罐.采用序贯法确定麻醉维持期间异氟醚的呼气末浓度,C组、D1组和D2组第1例患者异氟醚呼气末浓度分别设定为1.0%、0.8%和0.6%,当异氟醚呼气末浓度达到预设水平并维持15 min以上,且肌颤搐恢复到对照值90%以上时开始手术,相邻浓度差值为0.2%.于切皮时评估患者体动反应,以各交叉点异氟醚呼气末浓度的均数为MAC,并计算95%可信区间(CI).结果 C组、D1组和D2组入选病例分别为15、17和16例.异氟醚抑制切皮时体动反应的MAC及其95%CI分别为:C组(1.03±0.23)%(95%CI 0.83%～1.21%)、D1组(0.72±0.19)%(95%CI 0.58%～0.85%)、D2组(0.51±0.27)%(95%CI 0.30%～0.71%).与C组比较,D1组和D2组MAC降低(P＜0.01),D2组MAC明显低于D1组(P＜0.05).结论 右美托咪啶可明显降低异氟醚抑制切皮时患者体动反应的MAC,且与剂量有关.

Abstract：

Objective To investigate the effect of dexmedetomidine on minimum alveolar concentration (MAC) of isoflurane required to inhibit the body movement during skin incision. Methods Forty-eight ASA Ⅰ or Ⅱ patients aged 40-60 yr with body mass index of 22-27 kg/m2 undergoing elective upper abdominal surgery under general anesthesia were randomly divided into 3 groups: control group (group C, n = 15);low dose dexmedetomidine group (group D1, n = 17) and high dose dexmedetomidine group (group D2, n = 16). The patients were unpremedicated. Dexmedetomidine 0.4 and 0.8 μg/kg in normal saline (NS) 15 ml was infused over 15 min before induction of anesthesia in D1 and D2 groups respectively. Anesthesia was induced with fentanyl-propofol-succinylcholine. The patients were mechanically ventilated after tracheal intubation. Anesthesia was maintained with isoflurane. MAC of isoflurane was determined by up-and-down technique. The initial end-tidal isofiurane concentration was set at 1.0%, 0.8% and 0.6% in C, D1 and D2 groups respectively. Each time the end-tidal isoflurane concentration was increased/decreased by 0.2%. Skin incision was made after 15 min of equilibration, when the twitch height returned to more than 90% of its control value. Movement of body and limbs including swallowing and coughing were carefully looked for when skin incision was made. MAC of isoflurane was the mean of end-tidal concentration of isoflurane of each crossover pair, and 95 % CI was calculated. Results MAC of isoflurane was significantly decreased in D1 and D2 groups as compared with group C and in group D2 as compared with group D1( P ＜ 0.05 or 0.01 ). Conclusion Dexmedetomidine can significantly decrease MAC of isoflurane required to inhibit the body movement during skin incision in a dose-dependent manner.     

Atenolol may not modify anesthetic depth indicators in elderly patients — a second look at the data

PURPOSE: Decreased cardiac chronotropic response in elderly patients along with concomitant ss-blockade may suppress the autonomic responsiveness to surgical stimulation and subsequently obscure episodes of "light anesthesia". METHODS: We analyzed post hoc computerized data from our previous study evaluating the effects of perioperative atenolol administration. Bispectral index (BIS) and the performance of routine anesthetic depth indicators were analyzed in 45 patients undergoing abdominal surgery: Group I (n = 12), isoflurane/fentanyl/nitrous oxide in oxygen anesthesia; Group II (n = 16), isoflurane/fentanyl/nitrous oxide in oxygen with 10 mg atenolol intravenously prior to anesthesia; Group III (n = 17), isoflurane/fentanyl/nitrous oxide in oxygen with a maximum end-tidal isoflurane concentration of 0.4 vol.% and incremental doses of atenolol (5 mg intravenously stepwise). In all groups, blood pressure (BP) was maintained within +/- 20% of preoperatively defined baseline BP and heart rate (HR) between 50-80 beats x min(-1). BP, HR, and end-tidal isoflurane were tested for their potential to predict BIS using a previously described statistical model (P(K)). RESULTS: Although Group III patients received on average 39.5% less isoflurane compared with Group I patients (P = 0.006), and Groups II and III patients received on average 21% less fentanyl compared with Group I patients (P 相似文献   

Effects of Two Target-controlled Concentrations (1 and 3 ng/ml) of Remifentanil on MACBAR of Sevoflurane

Background: The aim of this prospective, randomized, double-blind study was to determine the effects of two different target-controlled concentrations of remifentanil (1 and 3 ng/ml) on the sevoflurane requirement for blunting sympathetic responses after surgical incision (MACBAR).

Methods: Seventy-four patients aged 20-50 yr, with American Society of Anesthesiologists physical status I, were anesthetized with propofol, cisatracurium, and sevoflurane with a mixture of 60% nitrous oxide in oxygen. Then, patients were randomly allocated to receive no remifentanil infusion (n = 27) or a target-controlled plasma concentration of 1 ng/ml (n = 27) or 3 ng/ml remifentanil (n = 20). Sympathetic responses to surgical incision (presence or absence of an increase in either heart rate or mean arterial blood pressure of 15% or more above the mean of the values measured during the 2 min before skin incision) were determined after a 20-min period of stable end-tidal sevoflurane and target-controlled remifentanil concentrations. Predetermined end-tidal sevoflurane concentrations and the MACBAR for each group were determined using an up-and-down sequential-allocation technique.

Results: The MACBAR of sevoflurane was higher in the group receiving no remifentanil (2.8% [95% confidence interval: 2.5-3.0%]) as compared with patients of the groups receiving 1 ng/ml (1.1% [0.9-1.3%]; P = 0.012) and 3 ng/ml remifentanil (0.2% [0.1-0.3%]; P = 0.006). When considering a minimum anesthetic concentration (MAC) value in this age population and the contribution of 60% nitrous oxide (0.55 MAC), the combined MACBAR values, expressed as multiples of the MAC, were 1.95 MAC, 1.1 MAC, and 0.68 MAC, in the three groups, respectively.     

Effects of halothane on intraocular pressure in anesthetized children

Intraocular pressure (IOP) measurements in children are usually performed under nitrous oxide and halothane anesthesia. We studied the effects of both time and end-tidal halothane concentration on IOP in 80 children (mean age +/- SD = 4.5 +/- 2.9 yr), to determine the most optimal time to make such measurements in anesthetized children. In 30 children the end-tidal halothane and nitrous oxide concentrations were kept constant while IOP was measured at 1-min intervals after the induction of anesthesia. Intraocular pressure did not change with time. In another 50 children IOP was measured immediately after induction, after 10 min of steady-state end-tidal halothane concentrations of both 0.5% and 1.0% in 66% nitrous oxide, and immediately after tracheal intubation. Intraocular pressure did not differ significantly at either halothane concentration but increased after tracheal intubation. We conclude that in patients anesthetized with halothane and nitrous oxide, IOP after induction remains constant over time and is not affected by end-tidal halothane concentrations up to 1.0% but is affected by tracheal intubation. Thus, the optimal time to measure IOP in children receiving up to 1% halothane in 66% nitrous oxide is during the first 10 min after induction, but before tracheal intubation.     

Xenon suppresses the hypnotic arousal in response to surgical stimulation.

STUDY OBJECTIVE: To evaluate the suppressive effects of xenon (Xe) on hypnotic arousal at skin incision. DESIGN: Prospective, randomized study. SETTING: Operating rooms at a university hospital. PATIENTS: 35 ASA physical status I and II patients presenting for elective lower abdominal surgery. INTERVENTIONS: Patients were randomly assigned to receive one of the following regimens: 1.3 minimum alveolar concentration (MAC) isoflurane, 1.3 MAC sevoflurane, 0.7 MAC Xe with 0.6 MAC sevoflurane, 1 MAC Xe with 0.3 MAC sevoflurane, or 0.7 MAC nitrous oxide (N2O) with 0.6 MAC sevoflurane (n = 7 each group). MEASUREMENTS AND MAIN RESULTS: The bispectral index (BIS) was measured at baseline, during anesthesia, and after skin incision. BIS increased significantly at skin incision from the values noted during anesthesia in the sevoflurane and N2O groups, whereas it remained stable at incision in the other three groups (mean change in BIS: 0 +/- 9 for isoflurane, 15 +/- 8 for sevoflurane, 5 +/- 6 for 0.7 MAC Xe, 4 +/- 11 for 1 MAC Xe, and 9 +/- 5 for N2O). CONCLUSIONS: Unlike N2O, Xe was able to suppress hypnotic arousal in response to surgical stimulation when administered with sevoflurane.