Effects of propofol and nitrous oxide on middle cerebral artery flow velocity and cerebral autoregulation

We studied the effects of adding 50% nitrous oxide to propofol anaesthesia administered by target-controlled infusion on middle cerebral artery flow velocity and autoregulatory indices derived from transient hyperaemic response tests. Nine healthy (ASA 1) adult patients scheduled to undergo elective surgery were recruited. A standardised anaesthetic comprising alfentanil 10 microg x kg(-1), propofol via a target-controlled infusion pump and vecuronium 0.1 mg x kg(-1) was used. Transcranial Doppler ultrasonography was used to measure middle cerebral artery (MCA) blood flow velocity and the transient hyperaemic response test was used to assess cerebral autoregulation. These measurements were performed while awake and then at an induction target concentration of propofol (the target at which consciousness was lost, mean 6.2 (SD 1.1) microg x ml(-1)). The measurements were repeated after the addition of 50% nitrous oxide to the breathing gas mixture. Propofol caused a significant decrease in MCA flow velocity and a significant increase in the strength of autoregulation. The addition of nitrous oxide had no significant effect on MCA flow velocity or cerebral autoregulation. These results suggest that addition of 50% nitrous oxide does not influence propofol-induced changes in cerebral haemodynamics.     

The effects of nitrous oxide on the auditory evoked potential index during sevoflurane anaesthesia

We have studied the effects of nitrous oxide on the auditory evoked response index (AAI-index) derived from the A-line monitoring device during sevoflurane anaesthesia in 21 patients undergoing minor ambulatory surgery. During sevoflurane anaesthesia with an AAI-index < 30, the addition or withdrawal of nitrous oxide in a concentration of 66% end tidal did not show any linear dose dependent change in AAI-index . However, comparing nitrous oxide > 40% to nitrous oxide < 10% end tidal concentration the AAI-index did decrease, p < 0.05. The AAI-index is either non-linear at deeper anaesthetic levels or is insensitive to the anaesthetic effects of nitrous oxide in terms of MAC-multiples.     

Choice of cuff inflation medium during nitrous oxide anaesthesia

Air, saline and a mixture of nitrous oxide and oxygen were used to inflate the cuffs of tracheal tubes inserted into three groups of patients, during nitrous oxide anaesthesia. Large increases in intracuff pressure were seen in the air group, but no morbidity resulted. The intracuff pressure decreased in the gas mix group and leaks occurred in some patients. Initial adjustment of cuff pressure was more difficult in the saline group but the pressure remained stable thereafter.     

Predictable nitrous oxide uptake enables simple oxygen uptake monitoring during low flow anaesthesia

The uptake rate of oxygen and nitrous oxide were studied during low flow anaesthesia with enflurane or isoflurane in nitrous oxide with either spontaneous or controlled ventilation. The excess gas flow and composition were analysed. The nitrous oxide uptake rate was in agreement with Severinghaus'formula _N20 1000.t^-0.5. The composition of excess gas was predictable and the following formula for oxygen uptake could be derived: O₂=fgO₂ -0.45 (fgN²O -(kg: 70.1000.t^-0.5)) where oxygen uptake rate (O₂, ml.min^-1) equals oxygen fresh gas flow (fgO₂) minus 0.45 times the difference between the fresh gas flow of nitrous oxide (fgN₂O), ml.min^-1 and estimated uptake of nitrous oxide. The equation assumes constant inspired gas concentrations of 30% oxygen and 65–70% nitrous oxide. The oxygen uptake rates calculated from this formula were in good agreement with measured uptake rates. Thus, continuous monitoring of oxygen uptake rates is possible by using only reliable flowmeters and analysis of inspried oxygen concentration.     

Cerebral state index during anaesthetic induction: a comparative study with propofol or nitrous oxide

BACKGROUND: Confidently predicting the depth of anaesthesia for the individual patient and independently of drug(s) type using EEG-based monitors has proven difficult. This open, randomized, explorative study of day surgical patients evaluates the ability of the Cerebral State Monitor (Danmeter AB, Odense, Denmark) of anaesthetic depth to identify loss of response (LOR) using either propofol or N(2)0 for induction. METHODS: In this open, randomized study, day surgical patients (n=10 in each group) were studied using the Cerebral State Index Monitor. After baseline measurements, induction to LOR was achieved with either repeated 30-mg boluses of propofol every second minute or with N(2)0 (after premedication 5 min before with 30 mg propofol) increased every other minute in 15% increments (max. 75%). Sedation level was evaluated every other minute using the Observer's Assessment of Alertness/Sedation scale. RESULTS: Baseline values were 91 (82-98) and 94 (82-100) for N(2)0 and propofol patients, respectively. During induction CSI decreased with increasing sedation in patients given propofol (P<0.001) but not in patients given nitrous oxide. Median value at LOR was 56 (40-76) and 95 (87-100) for the propofol and nitrous oxide group of patients, respectively. CONCLUSION: The Cerebral State Index(trade mark) behaves as other depth of anaesthesia monitors with a progressive decrease during propofol induction but loss of consciousness with N(2)0 results in no change in CSI.     

Recovery characteristics of propofol anaesthesia, with and without nitrous oxide: a comparison with halothane/nitrous oxide anaesthesia in children

Few studies have examined whether nitrous oxide influences the recovery characteristics of propofol anaesthesia. The present study examined the effect of nitrous oxide on the recovery characteristics of propofol anaesthesia, and compared these data with those for halothane/nitrous oxide anaesthesia. Sixty children aged 3–12 years were assigned at random to receive one of three maintenance regimens: propofol with or without nitrous oxide (70%) or halothane/nitrous oxide (70%). During propofol/N₂O anaesthesia, the infusion rate of propofol (180±39 μg·kg⁻¹·min⁻¹) required to maintain the mean arterial pressure and heart rate within 20% of the baseline values was significantly less than that during propofol/O₂ (220±37 μg·kg⁻¹·min⁻¹; P <0.005). The time from discontinuation of anaesthesia to eye-opening (11±6 min), to response to commands (12±6 min), and to return of full wakefulness (21±10 min) after propofol/N₂O were similar to those after propofol/O₂, but significantly less (by approximately 30%) than those after halothane ( P <0.05). The overall incidence of emesis after propofol/N₂O (53%) was greater than that after propofol/O₂ (17%, P <0.05) and comparable to that after halothane/N₂O (58%). These data suggest that N₂O has little effect on the rate of recovery after propofol, but significantly increases the incidence of postoperative emesis, thereby attenuating one of the main attributes of propofol anaesthesia.     

Effects of nitrous oxide on baroreflex gain and heart rate variability

Background:  Spontaneous baroreflex method allows continuous assessment of cardiovagal reflex function within resting blood pressure, but effects of nitrous oxide, per se , on the spontaneous baroreflex response remain unknown. This study was designed to determine the effects of nitrous oxide on spontaneous baroreflex gain and heart rate variability assessed by power spectral analysis in humans.
Methods:  Electrocardiogram and non-invasive blood pressure were monitored in 12 healthy volunteers before and during a 15-min inhalation of 67% nitrous oxide in oxygen, while spontaneous respiration was maintained. Least-square regression analysis relating R-R interval and systolic blood pressure was performed to obtain spontaneous baroreflex gains. Heart rate variability was analyzed using fast Fourier transformation.
Results:  Nitrous oxide did not significantly alter spontaneous baroreflex gains, which correlated well with high-frequency power (0.15–0.4 Hz) of heart rate variability before and during nitrous oxide inhalation.
Conclusion:  Our results indicate that (a) cardiovagal reflex response is not affected by nitrous oxide, per se , and (b) spontaneous baroreflex responses closely reflect beat-to-beat dynamic modulation of the cardiac cycle by the parasympathetic nervous system during inhalation of 67% nitrous oxide.     

Suppressive effect of nitrous oxide on motor evoked potentials can be reversed by train stimulation in rabbits under ketamine/fentanyl anaesthesia, but not with additional propofol

The effect of nitrous oxide on myogenic motor evoked potentials(MEPs) after multipulse stimulation is controversial. We investigatedthe effects of propofol in this paradigm. MEPs were elicitedelectrically by a single pulse and by trains of three and fivepulses in rabbits anaesthetized with ketamine and fentanyl.Nitrous oxide 30–70% was given and MEPs were recorded.After washout of nitrous oxide, propofol was given as a bolusof 10 mg kg^–1 followed by 0.8 (n=9) or 1.6 mg kg^–1 min^–1(n=8) as a continuous infusion. Nitrous oxide was then readministeredand MEPs were recorded. Without propofol, nitrous oxide significantlyreduced the amplitude of MEPs dose-dependently, but this effectwas reversed by multipulse stimulation. Administration of low-dosepropofol enhanced nitrous oxide-induced suppression, and thiseffect was reversed by five-pulse stimulation. However, high-dosepropofol produced a greater increase in suppression, such thateven five-pulse stimulation did not overcome the suppression.The results suggest that the degree of reversal of nitrous oxide-inducedMEP suppression produced by multipulse stimulation is affectedby the administration of propofol. Br J Anaesth 2001; 86: 395–402     

The effect of nitrous oxide on cerebral electrical activity

Recordings of cerebral electrical activity produced by the cerebral function analysing monitor ( CFAM ) were obtained from nine healthy volunteers breathing increasing concentrations of N2O in O2. Concentrations of 30 and 50% N2O produced significant reductions in CFAM trace amplitude. Withdrawal of N2O resulted in an increase in amplitude with an initial increase above the control level. There were no consistent changes in the frequency distribution of the weighted electroencephalographic signal with increasing concentrations of N2O.     

The effect of nitrous oxide on cerebral blood flow velocity in children anesthetized with propofol

BACKGROUND: Propofol for maintenance of anesthesia by continuous infusion is gaining popularity for use in pediatric patients. Nitrous oxide (N2O) has been shown to increase cerebral blood flow velocity (CBFV) in both children and adults. To determine the effects of N2O on middle cerebral artery blood flow velocity (Vmca) during propofol anesthesia in children, Vmca was measured with and without N2O using transcranial Doppler (TCD) sonography. METHODS: Thirty ASA I or II children aged 18 months to 6 years undergoing elective urological surgery were enrolled. Anesthesia comprised propofol aimed at producing an estimated steady-state serum concentration of 3 micro g.ml-1 and a caudal epidural block. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Each patient was randomized to receive a sequence of either Air/N2O/Air or N2O/Air/N2O in 35% oxygen. Fifteen min after each change in the N2O concentration, three measurements of cerebral blood flow velocity, blood pressure and heart rate were recorded. Ventilatory parameters and EtCO2 were kept constant throughout the study period. RESULTS: CBFV increased by 12.4% when air was replaced by N2O, and returned to baseline when N2O was subsequently removed. There was a 14% decrease in CBFV when N2O was replaced with air, which increased to baseline when air was subsequently replaced with N2O. Mean heart rate and blood pressure remained constant throughout the study period. CONCLUSION: The effects of nitrous oxide on CBFV are preserved in children during propofol anesthesia.     

Occupational exposure to sevoflurane, halothane and nitrous oxide during paediatric anaesthesia Waste gas exposure during paediatric anaesthesia

We report the findings of a study on exposure of operating room staff to sevoflurane, halothane and nitrous oxide during induction and maintenance of anaesthesia in children. Concentrations of anaesthetic agents in the operating theatre were measured directly by highly sensitive, photoacoustic infrared spectrometer during 20 anaesthetics. Samples were taken from the breathing zones of the anaesthetist and the circulating nurse. The operating theatre was of modern design with an air conditioning system providing 20 changes of air each hour. The threshold values of 100 ppm N₂O, 50 ppm isoflurane and 10 ppm halothane recommended by the United Kingdom Committee for Occupational Safety and Health (COSH) were exceeded in several cases for a short time during mask induction. After tracheal intubation, trace concentrations of sevoflurane, halothane and N₂O were mostly under the recommended levels and comparable to levels measured during adult anaesthesia.     

Echocardiographic assessment of the haemodynamic effects of propofol: a comparison with etomidate and thiopentone

The haemodynamic effects of propofol (2 mg/kg), etomidate (0.2 mg/kg) and thiopentone (4 mg/kg) were studied in 30 ASA 1 and 2 patients in whom anaesthesia had been induced with midazolam 0.1 mg/kg, fentanyl 5 micrograms/kg, vecuronium 0.1 mg/kg and atropine 10 micrograms/kg, and maintained with nitrous oxide in oxygen. Arterial pressure was measured directly and left ventricular diameters were determined by transoesophageal echocardiography. Systolic blood pressure after propofol and thiopentone and the end-systolic quotient (systolic pressure/end-systolic diameter), a measure of inotropy, decreased. Fractional shortening (end-diastolic-end-systolic diameter/end-diastolic diameter) decreased only in the thiopentone group. Diastolic blood pressure and end-diastolic diameter (a measure of preload) did not change in any of the groups, and the etomidate group showed no changes in the haemodynamic variables measured. Propofol shows simultaneous negative inotropy and afterload reduction, while thiopentone is exclusively negatively inotropic.     

Effects of nitrous oxide on cerebral haemodynamics and metabolism during isoflurane anaesthesia in man

Seven normoventilated and five hyperventilated healthy adults undergoing cholecystectomy and anaesthetized with methohexitone, fentanyl and pancuronium were studied with measurement of cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and quantified electroencephalography (EEG) under two sets of conditions: 1) 1.7% end-tidal concentration of isoflurane in air/oxygen; 2) 0.85% end-tidal concentration of isoflurane in nitrous oxide (N2O)/oxygen. The object was to study the effects of N2O during isoflurane anaesthesia on cerebral circulation, metabolism and neuroelectric activity. N2O in the anaesthetic gas mixture caused a 43% (P less than 0.05) increase in CBF during normocarbic conditions but no significant change during hypocapnia. CMRO2 was not significantly altered by N2O. EEG demonstrated an activated pattern with decreased low frequency activity and increased high frequency activity. The results confirm that N2O is a potent cerebral vasodilator in man, although the mechanisms underlying the effects on CBF are still unclear.