A comparison of the transient hyperemic response test and the static autoregulation test to assess graded impairment in cerebral autoregulation during propofol, desflurane, and nitrous oxide anesthesia.

The transient hyperemic response (THR) test has been used to assess cerebral autoregulation in anesthesia and intensive care. To date it has not been compared with the static autoregulation test for assessing graded changes in cerebral autoregulation. We compared the two tests during propofol, desflurane, and nitrous oxide anesthesia. Seven subjects were studied. For the THR test, changes in the middle artery blood flow velocity were assessed during and after a 10-s compression of the ipsilateral common carotid artery. Two indices of autoregulation--THR ratio (THRR) and strength of autoregulation (SA)--were calculated. For the test of static autoregulation, changes in the middle cerebral artery flow velocity after a phenylephrine-induces increase in mean arterial pressure were assessed, and the static rate of regulation (sROR) was calculated. The tests were performed before induction and after equilibrium at 0.5 minimum alveolar anesthetic concentration (MAC) and then at 1.5 MAC of desflurane. THRR, SA and sROR decreased significantly (P < 0.001) at 0.5 MAC and then at 1.5 MAC desflurane. CHanges in THRR and SA reflected the changes in sROR with a sensitivity of 100%. Implications: When compared with the established test of static autoregulation, the transient hyperemic response test provides a valid method for assessing graded impairment in cerebral autoregulation.     

The effects of nitrous oxide and oxygen on transient hyperemic response in human volunteers.

The aim of this study was to determine the effects of breathing 100% oxygen or 50% nitrous oxide in oxygen on the indices of cerebral autoregulation derived from the transient hyperemic response (THR) test in human volunteers. Data were analyzed from nine healthy subjects. Middle cerebral artery (MCA) blood flow velocity (FV) was measured by transcranial Doppler ultrasound, and the THR test was performed using 10-s compression of the common carotid artery. Continuous measurement of P(ETCO2) and expired fractions of oxygen (F(ETO2)) and nitrous oxide (F(ETN2O)) was established, and mean arterial pressure (MAP) was recorded at 2-min intervals. All measurements were performed while the volunteers were breathing room air and were repeated 10 min after achieving F(ETO2) >0.95 and 10 min after achieving F(ETN2O) 0.48-0.52. Two indices derived from the THR test, the transient hyperemic response ratio (THRR) and strength of autoregulation (SA), were used to assess cerebral autoregulation. P(ETCO2) and mean arterial pressure did not change significantly throughout the study period. Breathing 100% oxygen did not change MCA FV, THRR, or SA. Inhalation of nitrous oxide resulted in a marked and significant increase in the MCA FV (from 48+/-9 to 72+/-8 cm/s; mean +/- SD) and a significant decrease in the THRR (from 1.5+/-0.2 to 1.2+/-0.1) and the SA (from 1.0+/-0.1 to 0.8+/-0.1) (P<0.05 for all). We conclude that breathing 50% nitrous oxide in oxygen results in both a significant increase in MCA FV and impairment of transient hyperemic response. IMPLICATIONS: Our study suggests that nitrous oxide impairs cerebral autoregulation and may have implications for its use in neurosurgical anesthesia and for interpretation of the results from studies of anesthetics in which nitrous oxide is used in the background.     

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.     

Cerebral oxygen extraction and autoregulation during extracorporeal whole body hyperthermia in humans

BACKGROUND: The effects of hyperthermia on the human brain are incompletely understood. This study assessed the effects of whole body hyperthermia on cerebral oxygen extraction and autoregulation in humans. METHODS: Nineteen patients with chronic hepatitis C virus infection, not responding to interferon treatment, were subjected to experimental therapy with extracorporeal whole body hyperthermia at 41.8 degrees C for 120 min under propofol anesthesia (23 sessions total). During treatment series A (13 sessions), end-tidal carbon dioxide was allowed to increase during heating. During series B (10 sessions), end-tidal carbon dioxide was maintained approximately constant. Cerebral oxygen extraction (arterial to jugular venous difference of oxygen content) and middle cerebral artery blood flow velocity were continuously measured. Cerebral pressure-flow autoregulation was assessed by static tests using phenylephrine infusion and by assessing the transient hyperemic response to carotid compression and release. RESULTS: For treatment series A, cerebral oxygen extraction decreased 2.2-fold and cerebral blood flow velocity increased 2.0-fold during heating. For series B, oxygen extraction decreased 1.6-fold and flow velocity increased 1.5-fold. Jugular venous oxygen saturation and lactate measurements did not indicate cerebral ischemia at any temperature. Static autoregulation test results indicated loss of cerebrovascular reactivity during hyperthermia for both series A and series B. The transient hyperemic response ratio did not decrease until the temperature reached approximately 40 degrees C. Per degree Celsius temperature increase, the transient hyperemic response ratio decreased 0.07 (95% confidence interval, 0.05-0.09; P = 0.000). This association remained after adjustment for variations in arterial partial pressure of carbon dioxide, mean arterial pressure, and propofol blood concentration. CONCLUSION: Profound hyperthermia during propofol anesthesia is associated with decreased cerebral oxygen extraction, increased cerebral blood flow velocity, and impaired pressure-flow autoregulation, indicating transient partial vasoparalysis.     

The effect of sevoflurane on cerebral autoregulation in young children as assessed by the transient hyperemic response

The transient hyperemic response (THR) test is a simple, noninvasive technique to evaluate cerebral autoregulation using transcranial Doppler. It has not yet been used in studies involving children. In this study we evaluated this response in children undergoing general anesthesia using sevoflurane. Twenty ASA physical status I children undergoing elective urological surgery sequentially received sevoflurane at 0.5, 1.0, and 1.5 MAC in a randomized order. Analgesia was solely provided by caudal anesthesia. The right middle cerebral artery flow velocities before (F1), during (F2), and after (F3) a 10-s ipsilateral carotid artery compression were recorded. The THR ratios (THRR) (+/- sd) for 0.5 MAC, 1.0 MAC, and 1.5 MAC were 1.24 +/- 0.11, 1.16 +/- 0.09, and 1.13 +/- 0.07, respectively. The THRR was significantly different between 0.5 MAC versus 1.0 and 1.5 MAC, respectively (P < 0.05). However, no difference was detected between 1.0 and 1.5 MAC. A THRR of more than 1.09 has previously been accepted as the lower limit of a positive response. The results in this study suggest that THR is affected by sevoflurane in a dose-dependent fashion but is maintained at up to 1.5 MAC. This suggests cerebral autoregulation is preserved in children anesthetized with up to 1.5 MAC sevoflurane.     

Effects of Sevoflurane with and without Nitrous Oxide on Human Cerebral Circulation: Transcranial Doppler Study

Background: This study was designed to evaluate the effects of sevoflurane with and without nitrous oxide on human middle cerebral artery (MCA) flow velocity, cerebrovascular carbon dioxide reactivity, and autoregulation compared with the awake state using transcranial Doppler ultrasonography.

Methods: In 14 patients, the time-mean middle cerebral artery flow velocity (Vmca) was measured when the end-tidal carbon dioxide level was approximately 30, 40, and 50 mmHg under the following conditions: (1) awake; (2) with 2% (1.2 MAC) sevoflurane; and (3) with 1.2 MAC sevoflurane-60% nitrous oxide. In six other patients, the cerebrovascular autoregulation during anesthesia was determined using intravenous phenylephrine to increase blood pressure.

Results: Sevoflurane (1.2 MAC) significantly decreased Vmca compared with the awake value at each level of end-tidal carbon dioxide, whereas 1.2 MAC sevoflurane-60% nitrous oxide did not exert significant influence. The Vmca in normocapnic patients decreased from 69 cm/s to 55 cm/s with 1.2 MAC sevoflurane and then increased to 70 cm/s when nitrous oxide was added. Sevoflurane (1.2 MAC) with and without 60% nitrous oxide had a negligible effect on cerebrovascular carbon dioxide reactivity. A phenylephrine-induced increase of mean arterial pressure did not influence Vmca during anesthesia.     

Cerebral autoregulation during sevoflurane or isoflurane anesthesia: evaluation with transient hyperemic response]

We investigated dynamic cerebral autoregulation during N2O-O2/fentanyl anesthesia (baseline) plus 1.0 and 2.0 minimum alveolar anesthetic concentrations (MAC) of sevoflurane or isoflurane anesthesia in 14 patients undergoing non-neurosurgical operation. Cerebral blood flow velocity in the right middle cerebral artery (Vmca) was measured continuously using transcranial Doppler ultrasonography. At normocapnia, dynamic cerebral autoregulation was tested by transient hyperemic response (a response of Vmca after a brief compression of the ipsilateral common carotid artery). For quantitative comparisons, ratio of systolic Vmca before, to immediately after compression (THRR) was calculated. Values of THRR were 1.14 +/- 0.03 (mean +/- SD), 1.15 +/- 0.04, and 1.12 +/- 0.03 during baseline, 1.0, and 2.0 MAC sevoflurane anesthesia, respectively. THRR was not significantly different among the 3 conditions. In contrast, THRR values were 1.17 +/- 0.03, 1.07 +/- 0.02, and 1.01 +/- 0.01 during baseline, 1.0, and 2.0 MAC isoflurane anesthesia, respectively. THRR was significantly attenuated in a dose dependent manner during isoflurane anesthesia. These results indicate that dynamic cerebral autoregulation is preserved during 2.0 MAC sevoflurane anesthesia, but not during 1.0 MAC isoflurane anesthesia.     

Cerebral Oxygen Extraction and Autoregulation during Extracorporeal Whole Body Hyperthermia in Humans

Background: The effects of hyperthermia on the human brain are incompletely understood. This study assessed the effects of whole body hyperthermia on cerebral oxygen extraction and autoregulation in humans.

Methods: Nineteen patients with chronic hepatitis C virus infection, not responding to interferon treatment, were subjected to experimental therapy with extracorporeal whole body hyperthermia at 41.8[degrees]C for 120 min under propofol anesthesia (23 sessions total). During treatment series A (13 sessions), end-tidal carbon dioxide was allowed to increase during heating. During series B (10 sessions), end-tidal carbon dioxide was maintained approximately constant. Cerebral oxygen extraction (arterial to jugular venous difference of oxygen content) and middle cerebral artery blood flow velocity were continuously measured. Cerebral pressure-flow autoregulation was assessed by static tests using phenylephrine infusion and by assessing the transient hyperemic response to carotid compression and release.

Results: For treatment series A, cerebral oxygen extraction decreased 2.2-fold and cerebral blood flow velocity increased 2.0-fold during heating. For series B, oxygen extraction decreased 1.6-fold and flow velocity increased 1.5-fold. Jugular venous oxygen saturation and lactate measurements did not indicate cerebral ischemia at any temperature. Static autoregulation test results indicated loss of cerebrovascular reactivity during hyperthermia for both series A and series B. The transient hyperemic response ratio did not decrease until the temperature reached approximately 40[degrees]C. Per degree Celsius temperature increase, the transient hyperemic response ratio decreased 0.07 (95% confidence interval, 0.05-0.09; P = 0.000). This association remained after adjustment for variations in arterial partial pressure of carbon dioxide, mean arterial pressure, and propofol blood concentration.     

Cerebral hemodynamic response to the introduction of desflurane: A comparison with sevoflurane

Rapid increases in the inspired concentration of desflurane cause transient increases in heart rate and blood pressure. Desflurane also impairs cerebral autoregulation at clinical concentrations. Sevoflurane does not share these hemodynamic side effects. We compared the cerebral and systemic hemodynamic responses to the introduction of desflurane or sevoflurane after the induction of anesthesia with propofol. Twenty healthy adult patients scheduled for nonneurological surgery were recruited. After the induction of anesthesia with propofol, either desflurane or sevoflurane (n = 10 per group) was introduced at 7.2% or 2.2%, respectively, and increased to 10.8% or 3.3%, respectively, 2 min later. Middle cerebral artery blood flow velocity was measured continuously by using a 2-MHz transcranial Doppler ultrasound probe. Heart rate and blood pressure were recorded at 1-min intervals during the 12-min study period. Those patients receiving desflurane had significantly greater middle cerebral artery blood flow velocities, heart rates, and blood pressures than those receiving sevoflurane (P < 0.01). IMPLICATIONS: The introduction of desflurane after the induction of anesthesia leads to significant disturbances in cerebral and systemic hemodynamics suggesting loss of cerebral autoregulation and cerebral hyperemia. This may have implications for patients undergoing anesthesia for intracranial surgery.     

The influence of increasing concentrations of nitrous oxide on cerebral blood flow velocity in hypocapnic patients with brain tumours.

An increase of more than 50% in cerebral blood flow velocity in the middle cerebral artery was recently reported in hypocapnic volunteers, while inhaling 50% nitrous oxide. We measured cerebral blood flow velocity in the middle cerebral artery in 10 anaesthetized hypocapnic (ETCO2 = 25 mmHg) patients with brain tumours while administering increasing concentrations of nitrous oxide. At an end-tidal concentration of 50% and 70% nitrous oxide in oxygen, neither mean arterial pressure (base-line: 84 +/- 8 mmHg vs. (50% nitrous oxide): 82 +/- 9 mmHg and (70% nitrous oxide): 80 +/- 8 mmHg) nor cerebral blood flow velocity in the middle cerebral artery (base-line: 32 +/- 7 cm s-1 vs. (50% nitrous oxide): 34 +/- 8 cm s-1 and (70% nitrous oxide): 34 +/- 9 cm s-1) changed significantly. The data from our clinical investigation indicate that administration of increasing concentrations of nitrous oxide to already anaesthetized and hypocapnic patients does not change cerebral blood flow velocity in the middle cerebral artery.     

A bedside test for cerebral autoregulation using transcranial Doppler ultrasound

Summary Although disorders of cerebral autoregulation are commonly seen in neurosurgical disease, there is currently no test of autoregulation in widespread use that may be performed safely at the bedside. The presence of autoregulation, however, can be seen in the brief hyperemic response in the middle cerebral artery distribution following a transient manual carotid artery compression in the neck. This transient hyperemic response (THR) is readily measured with transcranial Doppler techniques, and therefore might serve as a qualitative marker of cerebral autoregulation.To evaluate the THR as a clinical tool, carotid compressions were performed during 172 TCD studies on 79 patients with neurosurgical disorders and on 10 patients without cerebral disease. The results were correlated with clinical status (e.g., Hunt-Hess Grade for subarachnoid hemorrhage and Glasgow Coma Score for trauma). There were no complications arising from the compressions. A separate assessment of autoregulation was made from TCD recordings obtained intraoperatively during 16 procedures and correlated to the pre-operative THRs. Autoregulation was further assessed in 4 patients during a hypotensive challenge, and again compared to the THRs.A strong correlation was seen between the THR results and clinical status. The THR was also strongly correlated with the intraoperative assessments, and all 4 patients receiving hypotensive challenges had abnormal THRs and demonstrated evidence of poor autoregulation during the challenge. None of the control patients had abnormal THRs.The THR arising from transient artery compression is readily detected with TCD techniques and correlates well with clinical status and other indicators of autoregulatory ability. The THR test can be safely performed at the bedside, uses noninvasive technology, and may emerge as a useful marker of cerebral autoregulation.     

不同麻醉方法对神经外科手术患者脑血管自身调节功能影响的比较

目的 比较不同麻醉方法对神经外科手术患者脑血管自身调节功能的影响.方法 拟行颅脑肿瘤切除术患者69例,ASA分级Ⅱ或Ⅲ级,年龄23～62岁,采用随机数字表法,将患者随机分为3组(n=23):异丙酚-瑞芬太尼复合麻醉组(PR组)、七氟醚.瑞芬太尼复合麻醉组(SR组)和异丙酚-七氟醚-瑞芬太尼复合麻醉组(PSR组).麻醉诱导:PR组和PSR组TCI异丙酚,血浆靶浓度为3μg/ml;SR组吸入8%七氟醚;3组均静脉注射瑞芬太尼1 mg/kg和阿曲库铵0.5 mg/kg.气管插管后机械通气,维持PETCO2 32～35 mm Hg.麻醉维持:PR组TCI异丙酚,血浆靶浓度2.0～3.5/μg/ml,SR组吸入1.5%～2.5%七氟醚,PSR组TCI异丙酚(血浆靶浓度1.5～3.0 μg/ml)复合吸入1%七氟醚,3组均TCI瑞芬太尼(血浆靶浓度2.0～4.5 ng/ml),静脉输注阿曲库铵6 μg·kg-1·min-1,维持听觉诱发电位指数值40～45.分别于麻醉诱导前(基础状态,T0)、气管插管后即刻(T1)、打开颅骨前即刻(T2)及开始缝皮时(T3)记录大脑中动脉时间-平均峰值流速,于相应时点压迫一侧颈总动脉7 s,计算脑短暂充血反应率(THRR),以反映脑血管自身调节功能.结果 与T0时比较,PR组T2时THRR升高,SR组T2,3时THRR降低(P<0.05),PSR组THRR差异无统计学意义(P>0.05).与PR组比较,SR组和PSR组THRR降低(P<0.05);与SR组比较,PSR组THRR升高(P<0.05).结论 异丙酚-瑞芬太尼复合麻醉可提高神经外科手术患者脑血管自身调节功能,七氟醚-瑞芬太尼复合麻醉可降低其脑血管自身调节功能,异丙酚-七氟醚-瑞芬太尼复合麻醉对其脑血管自身调节功能无影响.

Abstract：

Objective To compare the effect of different methods of anesthesia on cerebral autoregulation in patients undergoing neurosurgery.Methods Sixty-nine ASA Ⅱ orⅢ patients with brain tumor, aged 23-62 yr, scheduled for neurosurgery under general anesthesia, were randomly divided into 3 groups ( n = 23 each) : propofol-remifentanil group (group PR), sevoflurane-remifentanil group (group SR) and propofol-sevoflurane-remifentanil group (group PSR) . Anesthesia was induced with target-controlled infusion (TCI) of propofol (target plasma concentration3 μg/ml, PR and PSR groups) or inhalation of 8% sevoflurane (group SR) and iv injection of remifentanil 1 mg/kg and atracurium 0.5 mg/kg. The patients were mechanically ventilated after tracheal intubation. PETCO2 was maintained at 32-35 mm Hg. Anesthesia was maintained with TCI of propofol (target plasma concentration 2.0-3.5 μg/ml) in group PR, with inhalation of 1.5%-2.5% sevoflurane in group SR, with TCI of propofol (target plasma concentration 1.5-3.0 μg/ml) and inhalation of 1% sevoflurane in group PSR, and with TCI of remifentanil (target plasma concentration 2.0-4.5 ng/ml) and iv infusion of atracurium at 6 μg · kg-1 · min-1 in all groups. Auditory evoked potential index was maintained between 40-45. The middle cerebral artery time-average peak flow velocity was recorded before induction (baseline) , immediately after intubation, immediately before craniotomy and at the beginning of skin suture. The unilateral carotid artery was compressed for 7 s at the corresponding time points mentioned above. The transient hyperemic response ratio (THRR) was calculated to reflect cerebral autoregulation. Results Compared with the baseline value at T0, THRR was significantly increased at T2in group PR and decreased at T2,3 in group SR (P <0.05) ,while no significant change was found in THRR at T1-3in group PSR (P >0.05). The THRR was significantly lower in SR and PSR groups than in group PR, and higher in group PSR than in group SR ( P < 0.05). Conclusion Propofol-remifentanil anesthesia can improve cerebral autoregulation, sevoflurane-remifentanil anesthesia can reduce cerebral autoregulation, and propofol-sevofluraneremifentanil anesthesia exerts no effect on cerebral autoregulation in patients undergoing neurosurgery.     

Graded Hypercapnia and Cerebral Autoregulation during Sevoflurane or Propofol Anesthesia

Background: Hypercapnia abolishes cerebral autoregulation, but little is known about the interaction between hypercapnia and autoregulation during general anesthesia. With normocapnia, sevoflurane (up to 1.5 minimum alveolar concentration) and propofol do not impair cerebral autoregulation. This study aimed to document the level of hypercapnia required to impair cerebral autoregulation during propofol or sevoflurane anesthesia.

Methods: Eight healthy subjects received a remifentanil infusion and were anesthetized with propofol (140 [mu]g [middle dot] kg-1 [middle dot] min-1) and sevoflurane (1.0-1.1% end tidal) in a randomized crossover study. Ventilation was adjusted to achieve incremental increases in arterial carbon dioxide partial pressure (Paco2) until autoregulation was impaired. Cerebral autoregulation was tested by increasing the mean arterial pressure (MAP) from 80 to 100 mmHg with phenylephrine while measuring middle cerebral artery flow velocity by transcranial Doppler. The autoregulation index, which has a value ranging from 0 to 1, representing absent to perfect autoregulation, was calculated, and an autoregulation index of 0.4 or less represented significantly impaired autoregulation.

Results: The threshold Paco2 to significantly impair cerebral autoregulation ranged from 50 to 66 mmHg. The threshold averaged 56 +/- 4 mmHg (mean +/- SD) during sevoflurane anesthesia and 61 +/- 4 mmHg during propofol anesthesia (P = 0.03). Carbon dioxide reactivity measured at a MAP of 100 mmHg was 30% greater than that at a MAP of 80 mmHg.     

Graded hypercapnia and cerebral autoregulation during sevoflurane or propofol anesthesia

BACKGROUND: Hypercapnia abolishes cerebral autoregulation, but little is known about the interaction between hypercapnia and autoregulation during general anesthesia. With normocapnia, sevoflurane (up to 1.5 minimum alveolar concentration) and propofol do not impair cerebral autoregulation. This study aimed to document the level of hypercapnia required to impair cerebral autoregulation during propofol or sevoflurane anesthesia. METHODS: Eight healthy subjects received a remifentanil infusion and were anesthetized with propofol (140 microg. kg-1. min-1) and sevoflurane (1.0-1.1% end tidal) in a randomized crossover study. Ventilation was adjusted to achieve incremental increases in arterial carbon dioxide partial pressure (Paco2) until autoregulation was impaired. Cerebral autoregulation was tested by increasing the mean arterial pressure (MAP) from 80 to 100 mmHg with phenylephrine while measuring middle cerebral artery flow velocity by transcranial Doppler. The autoregulation index, which has a value ranging from 0 to 1, representing absent to perfect autoregulation, was calculated, and an autoregulation index of 0.4 or less represented significantly impaired autoregulation. RESULTS: The threshold Paco2 to significantly impair cerebral autoregulation ranged from 50 to 66 mmHg. The threshold averaged 56 +/- 4 mmHg (mean +/- SD) during sevoflurane anesthesia and 61 +/- 4 mmHg during propofol anesthesia (P = 0.03). Carbon dioxide reactivity measured at a MAP of 100 mmHg was 30% greater than that at a MAP of 80 mmHg. CONCLUSIONS: Even mild hypercapnia can significantly impair cerebral autoregulation during general anesthesia. There is a significant difference between propofol anesthesia and sevoflurane anesthesia with respect to the effect of hypercapnia on cerebral autoregulation. This difference occurs at clinically relevant levels of Paco2. When inducing hypercapnia, carbon dioxide reactivity is significantly affected by the MAP.     

Transcranial Doppler ultrasound study of the effects of nitrous oxide on cerebral autoregulation during neurosurgical anesthesia: a randomized controlled trial

OBJECT: Nitrous oxide has an adverse effect on cerebrovascular hemodynamics. Increased intracranial pressure, cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and reduced autoregulation indices have been reported, but their magnitudes are still being debated. This study was designed to evaluate the effect of N2O on CBF and autoregulatory indexes during N2O-sevoflurane anesthesia in a prospective randomized controlled series of patients. METHODS: Two groups of 20 patients were studied on the basis of the use of N2O in the anesthetic gas mixture. The transient hyperemic response test, which relies on transcranial Doppler ultrasound techniques, was used to assess cerebral hemodynamics. The time-averaged mean flow velocity, considered to be an index of actual CBF, increased significantly (p < 0.001) after introduction of N2O. The hyperemic response, considered as the index of autoregulatory potential, decreased significantly after introduction of N2O into the gas mixture (p < 0.001). CONCLUSIONS: The increase in CBF and the reduction in autoregulatory indices suggest caution in using N2O during sevoflurane anesthesia, especially in patients with reduced autoregulatory reserve and during neurosurgical interventions. Transcranial Doppler ultrasonography is an efficacious method to evaluate the effects of anesthetic agents on CBF.     

The effect of nitrous oxide on cerebral blood flow velocity in children anaesthetised with desflurane

The aim of this study was to determine the effect of nitrous oxide on cerebral blood flow velocity in children anaesthetised with desflurane. Eighteen healthy children scheduled for elective surgery were enrolled into the study. Anaesthesia was induced using sevoflurane, and a caudal block was performed following tracheal intubation. Anaesthesia was maintained with 1 age-adjusted MAC desflurane. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Each patient was randomised to receive a sequence of either air/nitrous oxide/air or nitrous oxide/air/nitrous oxide in 30% oxygen. Fifteen minutes after each change in the nitrous oxide concentration, three measurements of cerebral blood flow velocity, blood pressure and heart rate were recorded. Neither the addition nor removal of nitrous oxide caused any significant changes in middle cerebral artery blood flow velocity, heart rate or blood pressure. This may be due to a more potent cerebral vasodilatory effect of desflurane in children.     

Effects of target-controlled infusion of propofol on the transient hyperaemic response and carbon dioxide reactivity in the middle cerebral artery

The transient hyperaemic response (THR) of blood flow velocity in the middle cerebral artery (vmca), measured by transcranial Doppler ultrasonography (TCD), can be used to assess cerebral autoregulation. We have studied the effects of propofol administered by target- controlled infusion on vmca, THR and carbon dioxide reactivity. We studied 20 healthy adult patients undergoing elective surgery. A standardized anaesthetic comprising alfentanil 10 micrograms kg-1, propofol via a target-controlled infusor and vecuronium 0.1 mg kg-1 was used in both parts of the study. In the first part, THR tests were performed on 10 subjects while awake and then at an 'induction' target concentration of propofol (the target at which consciousness was lost, mean 6.7 (SD 1.1) micrograms ml-1). In the carbon dioxide study, reactivity was tested in 10 patients while awake and at the 'induction' target concentration of propofol by altering the end-tidal carbon dioxide partial pressure by 1 kPa either side of baseline. Propofol caused a significant decrease in vmca but indices of autoregulation, THR ratio and strength of autoregulation increased significantly. Propofol had no effect on carbon dioxide reactivity. These results suggest that propofol may have a beneficial effect on cerebral haemodynamics.      

Preserved CO(2) reactivity and increase in middle cerebral arterial blood flow velocity during laparoscopic surgery in children.

In adult patients, the creation of pneumoperitoneum (PP) by means of carbon dioxide (CO(2)) insufflation leads to an increase in cerebral blood flow velocity (CBFV), which is thought to be caused by hypercapnia. We evaluated whether PP leads to an increase of CBFV in children, and whether this increase is directly related to PP. The effects of PP on middle cerebral artery blood flow velocity were investigated in 12 children (mean age 3 yr, range 15-63 mo) undergoing laparoscopic herniorrhaphy under general anesthesia with sevoflurane and nitrous oxide/oxygen. CBFV was measured by using transcranial Doppler ultrasonography. During CO(2) insufflation, the end-tidal CO(2) concentration was kept constant by adjustment of ventilation by increasing minute volume. The CBFV increased significantly at an intraabdominal pressure of 12 mm Hg compared with baseline from 68 +/- 11 cm/s to 81 +/- 12 cm/s (P < 0.05). CO(2) reactivity remained in the normal range (4.0% +/- 1.9%/mm Hg) during PP. We conclude that the induction of PP leads to an increase in middle cerebral artery blood flow velocity in young children independent from hypercapnia, whereas CO(2) reactivity remains normal. IMPLICATIONS: Laparoscopic surgery is performed frequently in pediatric patients. Cerebral blood flow velocities increase during insufflation of the intraperitoneal cavity for minimally invasive surgery in children. The vasoreactivity as part of the cerebral autoregulation remains unaffected.     

The comparative effects of sevoflurane versus isoflurane on cerebrovascular carbon dioxide reactivity in patients with diabetes mellitus

The use of volatile anesthetics has been reported to alter cerebrovascular carbon dioxide (CO2) reactivity. We examined the comparative effects of sevoflurane versus isoflurane on cerebrovascular CO2 reactivity in 40 patients with diabetes mellitus. Anesthesia was maintained with either 1.0 minimum alveolar anesthetic concentration of sevoflurane or 1.0 minimum alveolar anesthetic concentration of isoflurane in 33% oxygen and 67% nitrous oxide. A 2.5-MHz pulsed transcranial Doppler probe was attached to the patient's head at the right temporal window for continuous measurement of mean blood flow velocity in the middle cerebral artery. After establishing baseline middle cerebral artery velocity values and cardiovascular hemodynamics, we increased end-tidal CO2 by decreasing ventilatory frequency by 2-5 breaths/min and repeated the measurements. These were then used to calculate absolute and relative CO2 reactivity. Absolute CO2 reactivity was less in insulin-treated patients with either sevoflurane or isoflurane compared with those patients on oral antidiabetic drugs or dietary therapy (sevoflurane group: diet = 2.6 +/- 0.6; oral antidiabetic drug = 2.5 +/- 0.8; insulin = 1.6 +/- 0.8*; isoflurane group: diet = 3.3 +/- i0.7; oral antidiabetic drug = 3.4 +/- 0.7; insulin = 1.9 +/- 0.7* cm.s(-1).mm Hg(-1); *P < 0.05, respectively). Relative CO2 reactivity showed a similar pattern in the diet-controlled and oral antidiabetic groups, absolute and relative CO2 reactivities were lower with sevoflurane versus isoflurane. Hence, we conclude that cerebrovascular CO2 reactivity in insulin-dependent patients is impaired under both sevoflurane and isoflurane anesthesia.     

The effect of nitrous oxide on cerebral blood flow velocity in children anaesthetised with sevoflurane

To determine the effects of nitrous oxide on middle cerebral artery blood flow velocity (CBFV) during sevoflurane anaesthesia in children, CBFV was measured using transcranial Doppler sonography in 16 ASA I or II children. Anaesthesia consisted of 1.0 MAC sevoflurane in 30% oxygen with intermittent positive pressure ventilation maintaining FEco2 at 38 mmHg (5.0 kPa) and a caudal epidural block using 0.25% bupivacaine 1.0 ml.kg-1. The remainder of the inspired gas was varied in one of two sequences either air/nitrous oxide/air or nitrous oxide/air/nitrous oxide. The results showed that CBFV decreased when nitrous oxide was replaced by air (p = 0.03) and returned to its initial value when nitrous oxide was reintroduced. CBFV increased when air was replaced by nitrous oxide (p = 0.04) and returned to its initial value when air was reintroduced. Mean heart rate and blood pressure remained constant. We conclude that nitrous oxide increases cerebral blood flow velocity in healthy children anaesthetised with 1.0 MAC sevoflurane.