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At least 19 recordsLinked to original sources
PubMed2005

Ambient isoflurane pollution and isoflurane consumption during intensive care unit sedation with the Anesthetic Conserving Device.

OBJECTIVE: To examine ambient isoflurane pollution, scavenging efficacy, and isoflurane consumption using the Anesthetic Conserving Device (ACD) for prolonged isoflurane sedation in the intensive care unit. DESIGN: Prospective observational study. SETTING: Multidisciplinary university intensive care unit. PATIENTS: Fifteen adult ventilator-dependent intensive care unit patients sedated with isoflurane for 12-96 hrs. INTERVENTIONS: Isoflurane was infused to the ACD for sedation of study subjects. Changing of the ACD, isoflurane syringe, and opening of the respiratory circuit were performed in a standardized fashion according to investigator instructions. Active scavenging of waste gas from the ventilator was performed in ten patients; in five patients no active scavenging was performed. MEASUREMENTS AND MAIN RESULTS: Continuous spectrophotometric measurement of ambient isoflurane pollution in parts per million (ppm) at 0.5 m from the patient's head and passive lapel dosimeter sampling for ten staff nurses over 8-hr shifts. Isoflurane requirement and agent consumption were registered in all patients. Spectrophotometric readings (0.1 +/- 0.2 ppm) were well below internationally recommended long-term exposure limits in all cases. Isoflurane peaks during nursing procedures were brief, infrequent, and of low amplitude. There was no observed difference between isoflurane trace levels with or without an active scavenging system in use. Passive dosimeter values were also low, ranging from undetectable to 0.16 ppm. Mean isoflurane consumption was 2.1 +/- 1.0 mL/hr. This is approximately one fourth of predicted and previously reported consumption of isoflurane with vaporizer-administered sedation in the intensive care unit setting. CONCLUSIONS: In the present setting, isoflurane via the ACD is an environmentally safe method of sedation provided users follow instructions for standardizing procedures with potential spillage of isoflurane. This method of sedation requires considerably less isoflurane than with traditional vaporizer technique.

Adult↗
PubMed1994

Nitrous oxide-isoflurane anesthesia causes more cerebral vasodilation than an equipotent dose of isoflurane in humans.

To compare the cerebral vascular and metabolic effect of an isoflurane-nitrous oxide mixture to an equipotent dose of isoflurane at 1.1 minimum alveolar anesthetic concentration (MAC), and to study the interaction between nitrous oxide and isoflurane anesthesia, we measured right middle cerebral artery blood flow velocity (V mca) and cerebral arteriovenous oxygen content difference (AVDO2) in six healthy patients during normocapnia and normothermia under the following sequence of steady-state anesthetic conditions: Condition A, 0.5 MAC of isoflurane, Condition B, 0.5 MAC of isoflurane + 0.6 MAC of N2O, Condition C, 1.1 MAC of isoflurane + 0.6 MAC of N2O, and Condition D, 1.1 MAC of isoflurane. The study entry sequence was randomized. V mca and AVDO2 during 1.1 MAC of isoflurane (Condition D) was 48 +/- 7 cm/s and 3.9 +/- 0.6 vol%, respectively. Substituting 0.6 MAC of isoflurane with an equipotent concentration of N2O (Condition B) resulted in an increase in both V mca and AVDO2 of approximately 20% (P < 0.05). These findings suggest that the increase in flow was accompanied by an even greater increase in metabolic rate. Adding 0.6 MAC of N2O to 1.1 MAC of isoflurane (Condition C) also increased V mca (P < 0.05). We conclude that N2O is a more potent cerebral vasodilator than an equipotent dose of isoflurane alone in humans.

Adult↗
PubMed2001

Effects of diazepam and flumazenil on minimum alveolar concentrations for dogs anesthetized with isoflurane or a combination of isoflurane and fentanyl.

OBJECTIVE: To determine the effect of a constant-rate infusion of fentanyl on minimum alveolar concentration (MAC) of isoflurane and to determine the interaction between fentanyl and a benzodiazepine agonist (diazepam) and antagonist (flumazenil) in isoflurane-anesthetized dogs. ANIMALS: 8 mixed-breed adult dogs. PROCEDURE: Dogs were anesthetized with isoflurane 3 times during a 6-week period. After a 30-minute equilibration period, each MAC determination was performed in triplicate, using standard techniques. Fentanyl was administered as a bolus (10 microg/kg of body weight, IV) that was followed by a constant infusion (0.3 microg/kg per min, IV) throughout the remainder of the experiment. After determining isoflurane-fentanyl MAC in triplicate, each dog received saline (0.9% NaCl) solution, diazepam, or flumazenil. After 30 minutes, MAC was determined again. RESULTS: Fentanyl significantly decreased isoflurane MAC (corrected to a barometric pressure of 760 mm Hg) from 1.80+/-0.21 to 0.85+/-0.14%, a reduction of 53%. Isoflurane-fentanyl-diazepam MAC (0.48+/-0.29%) was significantly less than isoflurane-fentanyl-saline MAC (0.79+/-0.21%). Percentage reduction in isoflurane MAC was significantly greater for fentanyl-diazepam (74%), compared with fentanyl-saline (54%) or fentanyl-flumazenil (61%). Mean fentanyl concentrations for the entire experiment were increased over time and were higher in the diazepam group than the saline or flumazenil groups. CONCLUSIONS AND CLINICAL RELEVANCE: Fentanyl markedly decreased isoflurane MAC in dogs. Diazepam, but not flumazenil, further decreased isoflurane-fentanyl MAC. Our results indicate that diazepam enhances, whereas flumazenil does not affect, opioid-induced CNS depression and, possibly, analgesia in dogs.

Adjuvants, Anesthesia↗
PubMed1995

[Three isoflurane preparations from various manufacturers. A comparison of isoflurane concentrations in fresh gas after vaporization with a Drager vaporizer type 19.3].

OBJECTIVES: The purpose of this study was to check the precision of the Dräger vaporizer model 19.3 when filled with three different preparations of isoflurane. METHODS: Six Dräger vaporizers model 19.3 calibrated with forene were filled with forene (Abbott), isoflurane (Lilly) and isoflurane (Pharmacia); gas output was measured by infrared absorption (Irina, Dräger) at vaporizer settings of 0.2, 0.4, 0.6, 0.8, 1.0, 1.5, 2.0, 2.5, 3.0, 3.5, 4.0 and 5.0 vol%, starting with a fresh gas flow of 2 1/min followed by 4, 6 and 12 1/min. Thus each of the three isoflurane preparations was checked in six different vaporizers and with four different fresh gas flows. RESULTS: Within the concentration range used in clinical practice there was no significant difference in the delivery of the three isoflurane preparations. Each of the six vaporizers produced a controllable and predictable concentration of the three preparations. CONCLUSION: Vaporizers of Dräger type 19.n calibrated with forene deliver the same predictable concentration of the volatile anaesthetic when filled with isoflurane from Lilly or isoflurane from Pharmacia instead of forene and may be used without impairment in patient safety. In addition, no specific calibration with one of the new isoflurane preparations is required.

Calibration↗
PubMed2006

Comparison of minimum alveolar concentration between intravenous isoflurane lipid emulsion and inhaled isoflurane in dogs.

BACKGROUND: As in inhaled isoflurane anesthesia, when isoflurane lipid emulsion (ILE; 8%, vol/vol) is intravenously administered, the primary elimination route is through the lungs. This study was designed to determine the minimum alveolar concentration (MAC) and the time course of washout of isoflurane for intravenously infused ILE by monitoring end-tidal isoflurane concentration. METHODS: Twelve healthy adult mongrel dogs were assigned randomly to an intravenous anesthesia group with 8% ILE or to an inhalation anesthesia group with isoflurane vapor. An up-and-down method and stimulation of tail clamping were used to determine MAC of 8% ILE by intravenous injection in the intravenous anesthesia group and MAC by the inhaled approach in the inhalation anesthesia group, respectively. Isoflurane concentration and partial pressure in end-tidal gas, femoral arterial blood, and jugular venous blood were measured simultaneously just before each tail clamping and during washout. RESULTS: The induction time in the intravenous anesthesia group (105 +/- 24 s) was shorter than that in the inhalation anesthesia group (378 +/- 102 s; P < 0.01). MAC of 8% ILE by intravenous injection (1.12 +/- 0.18%) was significantly less than MAC by the inhaled approach (1.38 +/- 0.16%; P < 0.05). No significant difference was found between the two groups in the time course of washout of isoflurane. CONCLUSION: The MAC of intravenous anesthesia with 8% ILE was less than that of inhalation anesthesia with isoflurane vapor in dogs.

Administration, Inhalation↗
PubMed1998

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 microg/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 microg/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 microg/kg caused no greater decrease in the MAC-BAR for desflurane (0.48 +/- 0.16 MAC) and isoflurane (0.40 +/- 0.30 MAC). CONCLUSIONS: Clinically attainable doses of desflurane and isoflurane, in 60% nitrous oxide (0.55 MAC), block the cardiovascular response to surgical incision at 1.3 MAC. Fentanyl given at 1.5 microg/kg decreases the MAC-BAR for each agent with no further decrease produced by 3 microg/kg fentanyl.

Adolescent↗
PubMed2007

Effect of isoflurane and other potent inhaled anesthetics on minimum alveolar concentration, learning, and the righting reflex in mice engineered to express alpha1 gamma-aminobutyric acid type A receptors unresponsive to isoflurane.

BACKGROUND: Enhancement of the function of gamma-aminobutyric acid type A receptors containing the alpha1 subunit may underlie a portion of inhaled anesthetic action. To test this, the authors created gene knock-in mice harboring mutations that render the receptors insensitive to isoflurane while preserving sensitivity to halothane. METHODS: The authors recorded miniature inhibitory synaptic currents in hippocampal neurons from hippocampal slices from knock-in and wild-type mice. They also determined the minimum alveolar concentration (MAC), and the concentration at which 50% of animals lost their righting reflexes and which suppressed pavlovian fear conditioning to tone and context in both genotypes. RESULTS: Miniature inhibitory postsynaptic currents decayed more rapidly in interneurons and CA1 pyramidal cells from the knock-in mice compared with wild-type animals. Isoflurane (0.5-1 MAC) prolonged the decay phase of miniature inhibitory postsynaptic currents in neurons of the wild-type mice, but this effect was significantly reduced in neurons from knock-in mice. Halothane (1 MAC) slowed the decay of miniature inhibitory postsynaptic current in both genotypes. The homozygous knock-in mice were more resistant than wild-type controls to loss of righting reflexes induced by isoflurane and enflurane, but not to halothane. The MAC for isoflurane, desflurane, and halothane did not differ between knock-in and wild-type mice. The knock-in mice and wild-type mice did not differ in their sensitivity to isoflurane for fear conditioning. CONCLUSIONS: gamma-Aminobutyric acid type A receptors containing the alpha1 subunit participate in the inhibition of the righting reflexes by isoflurane and enflurane. They are not, however, involved in the amnestic effect of isoflurane or immobilizing actions of inhaled agents.

Anesthetics, Inhalation↗
PubMed1993

Low-flow isoflurane-nitrous oxide anaesthesia offers substantial economic advantages over high- and medium-flow isoflurane-nitrous oxide anaesthesia.

Isoflurane consumption was studied for three different fresh gas flows in patients scheduled for major elective abdominal, urological or gynaecological surgery under general anaesthesia with an expected duration of 2 h or more. Thirty patients were randomly assigned to either high-flow anaesthesia using a partial rebreathing system without carbon dioxide absorption (Mapleson D) or medium- or low-flow anaesthesia using a circle system with carbon dioxide absorption. Patients were anaesthetised with isoflurane in 40% oxygen and 60% nitrous oxide. The amount of isoflurane consumed was measured with a precision scale. The total consumption of liquid isoflurane (mean +/- s.d.) during the first 2 h was 40.8 +/- 12.2 ml in the high-flow group, 18.5 +/- 5.4 ml in the medium-flow group and 7.9 +/- 2.2 ml in the low-flow group. The corresponding cost of isoflurane for the three groups was 214 Danish kroner (DKK) (19.5 pounds), 97 DKK (8.8 pounds) and 42 DKK (3.8 pounds), respectively. The calculated total cost of anaesthetics was 286 DKK (26 pounds), 155 DKK (14.1 pounds) and 91 DKK (8.3 pounds), respectively. In conclusion, low-flow isoflurane-nitrous oxide anaesthesia offers substantial economic advantages over high- and medium-flow isoflurane-nitrous oxide anaesthesia.

Adult↗
PubMed1993

Effects of isoflurane dose, duration of anoxia, and reoxygenation on isoflurane's preservation of energy balance in anoxic isolated hepatocytes.

We investigated how the protection of energy status by isoflurane in isolated hepatocytes varied with isoflurane dose, duration of anoxia, and reoxygenation. Hepatocytes were isolated from fed rats and incubated in Krebs buffer under O2/CO2 or N2/CO2 (95/5) for 30 or 90 min, followed by 5 or 30 min of reoxygenation. From measurements of adenosine tri-, di-, and monophosphate (ATP, ADP, AMP) in the cells, energy charge (= [ATP + 1/2 ADP]/[ATP + ADP + AMP]) was calculated to reflect the balance between ATP supply and demand, and total adenine nucleotide (= ATP + ADP + AMP) to indicate the potential maximum ATP level. During 30 min of anoxia, energy charge and total adenine nucleotide steadily increased with isoflurane dose from 0 to 2 minimum alveolar anesthetic concentration, then decreased from 2 to 3 minimum alveolar anesthetic concentration. In short incubations (30-35 min) at 1 minimum alveolar anesthetic concentration isoflurane, there was a modest decrease in energy charge during anoxia, partially prevented by isoflurane and completely reversed by reoxygenation, and no decrease in total adenine nucleotide. In long incubations (90-120 min), there were large decreases in both energy charge and total adenine nucleotide during anoxia, with partial and no reversal by reoxygenation, respectively. Isoflurane partly prevented decreases in both energy charge and total adenine nucleotide during both anoxia and reoxygenation. We conclude that at doses in the clinical range, isoflurane partially protected isolated hepatocytes against decreases in both energy charge and total adenine nucleotide occurring either during short (reversible) or long (irreversible) anoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1994

[Anesthesia with isoflurane in air and with isoflurane and nitrous oxide].

BACKGROUND: The aim of this study is to control the depth, the quality of recovery of total inhalation isoflurane anesthesia with or without nitrous oxide. DESIGN: Controlled comparative study was carried out on 51 patients, aged 40-54 yr, ASA 1, undergoing saphenectomy, in an University Clinic. METHODS: Induction: thiopental (3.5 mg kg), atracurium (0.6 mg kg) i.v. Patients were randomly assigned to: group 1 (26 patients), 5% isoflurane in air, by mask; group 2 (25 patients), 3% isoflurane and 60% N2O, by mask. Maintenance: group 1, 2% isoflurane in air; group 2, 1.2% isoflurane and 60% N2O. During anesthesia, consciousness and analgesia level were monitored by EEG Compressed Spectral Array, and clinical signs of pain by Evans' test; arousal time evaluation by "Time to correct response test". The subjective impressions, eventual dreams and recalls were collected using a standard set of questions one hour after the end of anesthesia and 24 hours later. One hour before anesthesia and two hours after the end of surgical procedures, a psychomotor performance recovery evaluation was performed using Zazzo's "deux barrages" test. DATA ANALYSIS: Student's "t" test. RESULTS: Adequate anesthetic depth was documented in all patients. Recovery time was statistically longer in isoflurane group (group 1 16.7 sd 2.2 minutes vs 10.3 sd 1.9 minutes group 2, p < 0.01). No patient reported recalls relative to anesthetic period. Two hours after recovery no significant differences in psychomotor performance tests were recorded. CONCLUSIONS: Isoflurane anesthesia in air, in adequate concentrations, provides a sufficient level of analgesia, hypnosis, amnesia, without clinical side effects.

Adult↗
PubMedDate not supplied

[Does propofol have advantages over midazolam and isoflurane? Comparative study of 2 total intravenous anesthesia techniques using midazolam and propofol, versus balanced anesthesia with isoflurane].

OBJECTIVES: To compare two techniques for total intravenous anesthesia (TIVA): midazolam-alfentanil-flumazenil and propofol-alfentanil, contrasting them with combined anesthesia (thiopental-isoflurane-alfentanil) and assessing the efficacy of flumazenil in continuous perfusion for preventing resedation in TIVA with midazolam. PATIENTS AND METHODS: The efficacy and clinical tolerance of the 3 anesthetic techniques with propofol, midazolam or isoflurane were studied in 63 patients undergoing elective breast, lumbar or gynecological surgery. Anesthetic induction was achieved with midazolam 0.3 mg/kg-1 (group M), propofol 2.5 mg/kg-1 (group P) or thiopental 3 mg/kg-1 (group I); all patients also received 50 micrograms/kg-1 alfentanil and vecuronium bromide 0.12 mg/kg-1/h-1. Maintenance was achieved with midazolam in perfusion at 0.12 mg/kg-1/h-1 (group M); propofol in perfusion at 7 mg/kg-1/h-1 and a pre-incision dose of 1.5 mg/kg-1 (group P); and isoflurane at 1.15% (group I). The 3 groups also received one pre-incision dose of alfentanil 25 micrograms/kg-1 and post-incision perfusion at 60 micrograms/kg-1/h-1. The infusion of alfentanil was changed by amounts of 20 micrograms/kg-1/h-1 in accordance with the patient's response to surgery. After surgery patients in group M received flumazenil 0.5 mg i.v. over 30 sec and a perfusion of flumazenil 0.5 mg over 60 min. Parameters indicating efficacy were: 1) total dose and timing of alfentanil; 2) number of instances of inadequate anesthesia; 3) peri-operative amnesia; 4) times of awakening and extubation after surgery, and 5) the number of patients in each group who required naloxone. Parameters indicating tolerance were: 1) hemodynamic variables; 2) the number of postoperative desaturations; 3) level of sedation, comprehension and motor coordination and orientation; 4) the "G/g detection" test and the memory recall test; 5) adverse side effects; 6) need for postoperative analgesia, and 7) evaluation of the anesthetic technique. RESULTS: The 3 techniques afforded effective control of hemodynamic response to intubation and surgical incision. Anesthetic maintenance was easy and safe with isoflurane and propofol. Higher doses of alfentanil, however, were needed with midazolam and we found a higher incidence of signs of superficial anesthesia. Reversion of midazolam with flumazenil 0.5 mg i.v. produced earlier awakening, although this was followed later by relapse into hypno-sedation that could not be prevented with a perfusion of flumazenil. Although recovery from anesthesia was slower with propofol than with isoflurane, we observed no differences in level of sedation, motor coordination and postoperative comprehension. Maintenance with isoflurane produced a higher incidence of adverse side effects such as tremors and nausea after surgery. CONCLUSIONS: None of the TIVA techniques proved superior in all the parameters studied during anesthetic maintenance when compared with balanced isoflurane-alfentanil, although the propofol-alfentanil combination was found to be superior to that of midazolam-alfentanil. After anesthesia, however, recovery was better with the association of propofol-alfentanil and adverse side effects were fewer. Flumazenil at the doses used was ineffective for preventing resedation due to midazolam.

Adolescent↗
PubMed1976

Lack of beta-adrenergic activity of isoflurane in the dog: a comparison of circulatory effects of halothane and isoflurane after propranolol administration.

The studies were undertaken to determine whether isoflurance inhalation is associated with a degree of beta-adrenergic action that is potentially important in clinical situations, and to compare the circulatory tolerance to isoflurane and halothane in dogs following beta blockade. We measured arterial and pulmonary artery pressure, left and right ventricular filling pressure, heart rate and cardiac output, and derived stroke volume and systemic and pulmonary vascular resistances in 13 mongrel dogs. The haemodynamic response to 1 MAC and 2 MAC isoflurane was studied in seven dogs and was similar before and after propranolol 0.1mg/kg i.v. In six dogs, propranolol 0.5mg/kg caused no significant changes in the circulatory response to 1 MAC and 2 MAC isoflurane or 1 MAC halothane. However, in three dogs, administration of 2 MAC halothane after propranolol 0.5mg/kg resulted in such profound circulatory depression as to preclude further study. These data suggest that (a) isoflurane possesses no clinically important beta-adrenergic stimulating activity; (b) there is no adverse drug interaction upon the circulation with the combination of isoflurane and propranolol; (c) in the presence of moderated profound beta-adrenergic blockade, 2 MAC isoflurane may be tolerated better than 2 MAC halothane.

Adrenergic beta-Agonists↗
PubMed1993

Cerebrovascular carbon dioxide reactivity during exposure to equipotent isoflurane and isoflurane in nitrous oxide anaesthesia.

We have studied the effects of hypocapnia on cerebrovascular changes in two MAC-equivalent anaesthetic regimens, using the transcranial Doppler technique as an index of cerebral blood flow (CBF) in 24 healthy ASA I patients undergoing spinal surgery. Eight of the patients were subjected to carbon dioxide reactivity challenges in the awake state. Before surgery, the other 16 patients received, in random order, either 1.15% isoflurane in oxygen or 0.5% isoflurane with 70% nitrous oxide. Carbon dioxide reactivity was calculated for each group as the increase in flow velocity per kPa change in PE'CO2 (cm s-1 kPa-1). It was significantly greater for the isoflurane group (14.09 (SD 2.44) cm s-1 kPa-1) and significantly less for the isoflurane-nitrous oxide group (7.95 (1.32) cm s-1 kPa-1) compared with the awake group (11.24 (0.95) cm s-1 kPa-1). We conclude that cerebrovascular responsiveness to changes in arterial carbon dioxide concentration is influenced markedly by the anaesthetic procedure. Hyperventilation is more likely to affect CBF during isoflurane anaesthesia than during an MAC-equivalent isoflurane-nitrous oxide anaesthesia.

Adult↗
PubMed1994

Overpressure isoflurane at caesarean section: a study of arterial isoflurane concentrations.

In this study we have measured arterial concentrations of isoflurane obtained during Caesarean section in two groups of patients. Patients in group 1 received 1% isoflurane throughout operation, whilst those in group 2 received 2% isoflurane for the first 5 min, 1.5% for the next 5 min and 0.8% thereafter. We found that arterial isoflurane concentrations were significantly greater in group 2 than in group 1 (ANOVA, P < 0.05). Isoflurane concentrations greater than 30 micrograms ml-1 were achieved rapidly in most patients in both groups, but there was a large scatter of results. The isoflurane concentration at which awareness or recall may occur is not known, but an "overpressure" technique as described for patients in group 2 may result in fewer patients being at risk of awareness.

Adolescent↗
PubMed2001

[Effects of combined transdermal acupoint electric stimulation and isoflurane anesthesia on isoflurane-induced hypotension and tissue oxygen metabolism in patients undergoing craniotomy].

OBJECTIVE: To observe the effects of combined transdermal acupoint electric stimulation and isoflurane anesthesia on isoflurane-induced hypotension and tissue oxygen metabolism in patients undergoing craniotomy. METHODS: Forty-two patients with brain tumor of ASA physical status I or II and scheduled for elective surgery were randomly divided into two groups. The craniotomy was undergoing in Group A with isoflurane anesthesia, while in Group B, with combined transdermal acupoint electric stimulation (TAES) and isoflurane anesthesia. Isoflurane induced hypotension was performed in both groups by augmenting the concentration of isoflurane to lower the mean arterial pressure than before anesthesia for 30%-40% and maintain for 30-45 mins. The tissue oxygen metabolism, blood gas and arterial lactic acid level before, during and after hypotension were monitored by Swan-Ganz floating catheterization. RESULTS: As compared with before hypotension, the pulmonary arterial and mixed with venous blood oxygen saturation lowered and oxygen supply lowered, and oxygen uptake increased significantly in both groups (P < 0.05), but the extent of changes in oxygen metabolic criteria in Group B were all lesser than those in Group A (P < 0.05). CONCLUSION: Combined acupoint electric stimulation and general anesthesia could maintain the tissue oxygen supply and demand balance better in the isofluraneinduced hypotension process.

Acupuncture Points↗
PubMed1985

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.

Adult↗