Esmolol blunts the cerebral blood flow velocity increase during emergence from anesthesia in neurosurgical patients

Cerebral hyperemia has been demonstrated during emergence from anesthesia in neurosurgical patients, but its mechanism is speculative. We performed this study to test the hypothesis that this could be attributed to sympathetic overactivity. Thirty neurosurgical patients were included in a prospective, randomized, double-blinded study comparing esmolol, a short-acting beta-blocker, and a placebo. Esmolol (0.3 mg. kg(-1). min(-1)) was infused from the end of anesthesia to 15 min after extubation. Cerebral blood flow velocity (CBFV), mean arterial blood pressure, and heart rate were recorded before anesthesia, during anesthesia after surgery, at extubation, and 5-60 min after extubation. Cardiac output (COe) was estimated by using an esophageal Doppler from anesthesia to 60 min after extubation. CBFV, COe, and heart rate were significantly lower in the esmolol group. Mean arterial blood pressure was comparable between the groups. There was no correlation between CBFV and COe at any time point during the study. In conclusion, esmolol blunted the CBFV increase during emergence, confirming that sympathetic overactivity contributes to cerebral hyperemia during neurosurgical recovery. IMPLICATIONS: Esmolol blunted the postoperative increase in cerebral blood flow velocity in neurosurgical patients. The origin of sympathetic hyperactivity and its potential deleterious consequences require further study.     

Cerebral blood flow velocity increases when propofol is changed to desflurane, but not when isoflurane is changed to desflurane in children

BACKGROUND: Children may exhibit delayed emergence following maintenance of anesthesia with propofol or isoflurane. Desflurane is often used towards the end of procedures to facilitate emergence. This study evaluated the effect on middle cerebral artery blood flow velocity (Vmca) in anesthetized children when propofol or isoflurane was substituted with desflurane. METHODS: Forty-two healthy children aged 1-6 years were enrolled. A standardized anesthetic induction was used. Anesthesia was maintained with remifentanil (0.5 microg.kg(-1) bolus followed by an infusion of 0.2 microg.kg(-1).min(-1)) and a randomly selected sequence of propofol/desflurane/propofol, desflurane/propofol/desflurane, isoflurane/desflurane/isoflurane or desflurane/isoflurane/desflurane. Propofol was administered to maintain a steady-state serum concentration of 3 microg.ml(-1). Desflurane and isoflurane were administered at age-corrected 1 MAC. Hemodynamic stability was maintained. Transcranial Doppler sonography was used to measure Vmca. Hemodynamic variables as well as Vmca were measured 30 min after skin incision and repeated 30 min after each change in anesthetic maintenance agent. RESULTS: The mean age and weight was 2.3 +/- 1.3 years and 13.0 +/- 3.7 kg, respectively. The Vmca (mean) increased by 35% from 37.7 +/- 10.5 cm s(-1) to 57.8 +/- 14.6 cm s(-1) (P < 0.0001) when propofol was changed to desflurane but was unaffected when desflurane replaced isoflurane. CONCLUSION: When propofol is changed to desflurane, cerebral blood flow velocity increases significantly in normal children. This cerebral vasodilatory effect may have important implications in the neurosurgical setting.     

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

BACKGROUND: Cerebrovascular stability and rapid anesthetic emergence are desirable features of a neuroanesthetic regimen. In this randomized crossover study the effect of a low-dose remifentanil infusion on cerebral blood flow velocity (CBFV) in children anesthetized with propofol was evaluated. METHODS: Twenty healthy children aged 1-6 years undergoing urological surgery were enrolled. Following face mask induction with sevoflurane, anesthesia was maintained with a standardized propofol infusion. Rocuronium was used to facilitate tracheal intubation and normothermia, and normocapnia were maintained. All children received a caudal epidural block, and a transcranial Doppler probe was placed to measure middle cerebral artery blood flow velocity (Vmca). Each patient received a remifentanil regimen of 0.5 microg x kg(-1) followed by 0.2 microg x kg(-1) x min(-1) in a predetermined order of remifentanil + propofol or propofol alone. Vmca, mean arterial pressure (MAP) and heart rate (HR) were recorded simultaneously at equilibrium with and without remifentanil. RESULTS: The combination of remifentanil and propofol caused an 8.1% decrease in MAP (P = 0.0005) and an 11.8% decrease in HR (P < 0.0001) compared with propofol alone. Vmca was not different between the two groups (P = 0.4041). CONCLUSION: The addition of remifentanil to propofol anesthesia in children causes a reduction in MAP and HR without affecting CBFV. This may imply that cerebral blood pressure autoregulation is preserved in children under propofol and remifentanil anesthesia.     

The effects of propofol on cerebral blood flow in correlation to cerebral blood flow velocity in dogs

This study correlates the effects of propofol on cerebral blood flow (CBF) and middle cerebral artery blood flow velocity in dogs. CBF was measured using radioactive microspheres. Cerebral oxygen consumption (CMRO2) was measured with each CBF determination. Blood flow velocity was measured through a transtemporal window using a pulsed 8 MHz transcranial Doppler ultrasound system (TCD). Electroencephalogram (EEG) was continuously recorded over both cerebral hemispheres. Cardiac output (CO) was measured using an electromagnetic flow probe placed on the pulmonary artery. Baseline measures were made in all dogs (n = 11) with 0.7% isoflurane end tidal and 50% N2O in O2. There were two treatment groups. In group 1 (n = 6), propofol (0.8 mg/kg/min) was infused and a second measurement made at induction of EEG burst suppression (12 +/- 2 min). CBF and CMRO2 decreased by 70% and mean blood flow velocity decreased by 60%. Blood pressure, heart rate, and CO did not change. Propofol infusion was discontinued and all parameters were measured following recovery of EEG to baseline activity (48 +/- 9 min). CBF and blood flow velocity increased 35 and 25%, respectively, and CMRO2 increased by 32% during this period. A second propofol infusion (0.8 mg/kg/min) was started and all cerebral and systemic hemodynamic parameters were again determined at induction of EEG burst suppression (12 +/- 2 min). CBF decreased 35% and blood flow velocity decreased 25% to levels seen during the first propofol infusion. Over the entire study, changes in CBF correlated with changes in blood flow velocity (r = 0.86, p < 0.05). In group 2 (n = 5), four control measures were made at the same time intervals as in group 1. Baseline CBF and blood flow velocity were lower in group 2 compared to group 1 but these measures did not change over time. Our results show that propofol produces marked decreases in CBF in dogs and that these changes are closely correlated with CBF velocity.     

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.     

The effects of sevoflurane and halothane anesthesia on cerebral blood flow velocity in children

We compared cerebral blood flow velocity during anesthesia with sevoflurane and halothane in 23 children admitted for elective surgery (age, 0.4-9.7 yr; median age, 1.9 yr; ASA physical status I-II). Inhaled induction was performed in a randomized sequence with sevoflurane or halothane. Under steady-state conditions, cerebral blood flow velocity (systolic [V(s)], mean [V(mn)], and diastolic [VD]) were measured by a blinded investigator using transcranial pulsed Doppler ultrasonography. The anesthetic was then changed. CBFV measurements were repeated after washout of the first anesthetic and after steady-state of the second (equivalent minimal alveolar concentration to first anesthetic). The resistance index was calculated. VD and V(mn) were significantly lower during sevoflurane (V(mn) 1.35 m/s) than during halothane (V(mn) 1.50 m/s; P = 0.001), whereas V(s) was unchanged. The resistance index was lower during halothane (P < 0.001). Our results indicate lower vessel resistance and higher mean velocity during halothane than during sevoflurane. IMPLICATIONS: The mean cerebral blood flow velocity is significantly decreased in children during inhaled anesthesia with sevoflurane than during halothane. This might be relevant for the choice of anesthetic in children with risk of increased intracranial pressure, neurosurgery, or craniofacial osteotomies.     

Physical exercise increases middle cerebral artery blood flow velocity

The effect on the middle cerebral artery blood flow velocity (V_MCA) of moderate and hard physical exercise on an ergometer cycle was examined in 10 healthy volunteers using transcranial Doppler sonography (TCD). During exercise, the heart rate increased by 136% and the systolic blood pressure by 37% (mean values). During initial moderate exercise, V_MCA increased by 51%; in a following period of maximal physical work, V_MCA decreased again by 20% in 9 of 10 volunteers although the heart rate continued to increase by 10% and the systolic blood pressure by 5% (mean values).Constriction of the MCA may explain the initial increase of V_MCA, suggesting a role for large cerebral arteries in autoregulation. Our data indicate that the subsequent decrease of V_MCA is caused by arteriolar constriction, a likely cause of which was hyperventilation during the excessive work period.     

Intravenous administration of flurbiprofen does not affect cerebral blood flow velocity and cerebral oxygenation under isoflurane and propofol anesthesia

Flurbiprofen, a nonsteroidal antiinflammatory drug (NSAID), has been used to treat rheumatic and osteoarthritic pain and to reduce postoperative pain. Although other NSAIDs, such as indomethacin, reduce cerebral blood flow (CBF), the effect of flurbiprofen on CBF is unknown. In the present study, we investigated the effects of flurbiprofen on cerebral blood flow velocity (CBFV) and cerebral oxygenation under isoflurane or propofol anesthesia. Forty-eight patients undergoing orthopedic or abdominal surgery were enrolled. Patients were randomly allocated to receive either propofol (target control infusion: target site effect concentration 3 microg/mL) or isoflurane (1 MAC) for maintenance of anesthesia. In each group (n = 12), 1 mg/kg of flurbiprofen (PROP-F and ISO-F groups) or 0.1 mL/kg saline (PROP-S and ISO-S groups) was administered i.v. for 5 min. During and after the administration of flurbiprofen or saline, cerebral oxygenation variables (tissue oxygen index [TOI], total hemoglobin change [Delta cHb], oxygenated hemoglobin changes [Delta O(2)Hb], and deoxygenated hemoglobin changes [Delta HHb]), and middle cerebral artery flow velocity (Vmca) were measured using a cerebral oximeter (NIRO 300) and transcranial Doppler, respectively, from 5 min before study drug administration to 60 min post-administration. Before the administration of flurbiprofen, control values of TOI in the ISO-S and ISO-F groups were significantly higher than those in the PROP-S and PROP-F groups, respectively (ISO-S versus PROP-S, 67% +/- 4% versus 60% +/- 7%; IOS-F versus PROP-F, 69% +/- 4% versus 63% +/- 8%; P < 0.05). However, values of TOI, Delta cHb, Delta O(2)Hb, Delta HHb, and Vmca did not change significantly during and after the administration of flurbiprofen under propofol or isoflurane anesthesia, and these values were similar to those during and after the administration of saline in the same anesthesia group. These data indicate that flurbiprofen does not affect CBFV and cerebral oxygenation under propofol or isoflurane anesthesia. IMPLICATIONS: Indomethacin, a nonsteroidal antiinflammatory drug (NSAID), has been demonstrated to reduce cerebral blood flow (CBF). The CBF effects of flurbiprofen, another NSAID, are unknown. We investigated cerebral blood flow velocity (CBFV) and cerebral oxygenation during and after the administration of flurbiprofen under isoflurane and propofol anesthesia. We found that flurbiprofen had no effect on CBFV and cerebral oxygenation.     

Propofol decreases cerebral blood flow velocity in anesthetized children

PURPOSE: Propofol, by virtue of its favourable pharmacokinetic profile, is suitable for maintenance of anesthesia by continuous infusion during neurosurgical procedures in adults. It is gaining popularity for use in pediatric patients. To determine the effects of propofol on cerebral blood flow in children, middle cerebral artery blood flow velocity (Vmca) was measured at different levels of propofol administration by transcranial Doppler (TCD) sonography. METHODS: Twelve ASA I or II children, aged one to six years undergoing elective urological surgery were randomized to receive one of two propofol dosing regimens. Half of the patients received propofol in an escalating fashion, initially targeting an estimated steady-state serum concentration of 3 microg x mL-1, which was then doubled. The other half received propofol designed initially to target the high concentration followed by the lower one. In each child anesthesia was induced and maintained with propofol according to the protocol, rocuronium was given to facilitate tracheal intubation, and a caudal epidural block was performed. A TCD probe was placed appropriately to measure Vmca. Cerebral blood flow velocity (CBFV), mean arterial pressure (MAP) and heart rate (HR) were recorded simultaneously at both levels of propofol administration. RESULTS: Twelve patients were studied. At the higher estimated target serum propofol concentration there were significant decreases in Vmca (17%, P < 0.001), MAP (6%, P < 0.002) and HR (8%, P < 0.05) when compared to the lower targeted concentration. CONCLUSION: This study shows that a higher rate of propofol infusion is associated with lower CBFV and MAP values in children. Propofol's cerebral vasoconstrictive properties may be responsible for this finding.     

Milrinone increases middle cerebral artery blood flow velocity after cardiopulmonary bypass

OBJECTIVE: To evaluate the effects of milrinone on middle cerebral artery blood flow velocity (Vmca) and pulsatility index (PI) during normocapnia and hyperventilation in adults after cardiopulmonary bypass (CPB). DESIGN: A prospective study. SETTING: University-affiliated hospital and Veterans Affairs Medical Center. PARTICIPANTS: Twenty-five adults with left ventricular ejection fraction >40% undergoing coronary artery bypass graft surgery. INTERVENTIONS: After separation from CPB, using transcranial Doppler ultrasonography, peak and mean Vmca and PI were recorded before and after the administration of 50 microg/kg of milrinone under normocapnia and with hyperventilation. MEASUREMENTS AND MAIN RESULTS: Heart rate, arterial blood pressure, central venous pressure, and cardiac output were documented after each study period. Compared with baseline, milrinone increased peak Vmca by 20%, increased mean Vmca by 19%, and decreased PI by 16% (p < 0.001). Before the administration of milrinone, hyperventilation decreased peak Vmca by 20%, decreased mean Vmca by 26%, and increased PI by 24% (p < 0.01). After milrinone administration, hyperventilation also decreased peak Vmca by 22%, decreased mean Vmca by 21%, and increased PI by 19% (p < 0.01). Milrinone increased cardiac index and decreased mean arterial pressure and systemic vascular resistance (p < 0.05); however, heart rate and central venous pressure remained unchanged. CONCLUSIONS: The administration of milrinone increases cerebral blood flow after CPB most likely as a result of cerebral vasodilation. The response to hyperventilation seems to be partially preserved.     

Phenylephrine increases regional cerebral blood flow following hemorrhage during isoflurane-oxygen anesthesia

Using the radioactive microsphere technique regional cerebral blood flow (rCBF) and total CBF (tCBF) were examined in rats at three time periods: baseline (CBF1) during 1.5 MAC inspired isoflurane-oxygen anesthesia, CBF2; during 1.5 MAC inspired isoflurane anesthesia combined with hypotension induced by hemorrhage and CBF3; during isoflurane and hemorrhage plus phenylephrine infused to restore mean arterial pressure (MAP) to baseline. For CBF1 MAP was 89 +/- 3 mmHg (mean +/- SEM, n = 9) with PaCO2 44 +/- 1 mmHg. For CBF2 following graded hemorrhage MAP was 48 +/- 2 mmHg and PaCO2 43 +/- 1 mmHg. For CBF3 MAP was 93 +/- 2 and PaCO2 45 +/- 1 mmHg, following infusion of phenylephrine (PE) at 13.9 +/- 4.0 micrograms.kg-1.min-1. Total CBF1 was 1.84 +/- 0.18 ml.g-1.min-1, tCBF2 1.32 +/- 0.09 ml.g-1.min-1 (P less than 0.05 vs. tCBF1) and tCBF3 2.60 +/- 0.18 (P less than 0.05 vs. tCBF1 and 2). For tCBF3 hemoglobin concentration had decreased 23% from 14.2 +/- 0.2 g.100 ml-1 to 11.0 +/- 0.5 g.100 ml-1 (P less than 0.05). Regional CBF decreased significantly in seven of 12 regions examined from CBF1 to CBF2 and was significantly higher in all regions for CBF3. For CBF1-3 infratentorial blood flows (cerebellar and brain stem) were significantly higher than flows to the supratentorial structures (cerebral cortical and basal ganglia). During isoflurane anesthesia, phenylephrine infused to support MAP following hemorrhagic hypotension effectively maintains rCBF and tCBF. There is no indication that phenylephrine infused to increase MAP following hemorrhage results in cerebral vasoconstriction in rats anesthetized with isoflurane.     

A comparison of propofol and sevoflurane anaesthesia: effects on aortic blood flow velocity and middle cerebral artery blood flow velocity

We compared systemic (aortic) blood flow and cerebral blood flow velocity in 30 patients randomly allocated to receive either propofol or sevoflurane anaesthesia. Cerebral blood flow velocity (CBFv) was measured in the middle cerebral artery using transcranial Doppler. Systemic blood flow velocity (SBFv) was measured in the aorta using transthoracic Doppler sonography at the level of the aortic valve. Bispectral index (BIS) was used to measure the depth of anaesthesia. Measurements were made in the awake patient and repeated during propofol or sevoflurane anaesthesia, with BIS measurements of 40-50. The effects of SBFv on CBFv were estimated by calculating the cerebral/systemic blood flow velocity-index (CsvI). A CsvI value of 100 indicating a 1 : 1 relationship between CBFv and SBFv. The results demonstrated that propofol anaesthesia produced a significantly greater reduction in CsvI than did sevoflurane anaesthesia [propofol: 60 (19); sevoflurane: 83 (16), p = 0.009, t-test]. This suggests a direct reduction in CBFv independent of SBFv during propofol anaesthesia. The greater reduction of CBFv occurring during propofol anaesthesia may be due to lower cerebral metabolic demand compared with sevoflurane anaesthesia at comparable depths of anaesthesia.     

Fentanyl is more effective than remifentanil at preventing increases in cerebral blood flow velocity during intubation in children

PURPOSE: Controlling the cerebral and systemic hemodynamic responses to laryngoscopy and tracheal intubation may play a role in determining clinical outcome in pediatric neurosurgical patients. This study compared the effects of remifentanil and fentanyl on cerebral blood flow velocity (CBFV) and hemodynamic profile during laryngoscopy and tracheal intubation in children under sevoflurane anesthesia. METHODS: Sixty healthy children aged two to six years undergoing dental surgery under general anesthesia were enrolled. Each child was randomly assigned to receive a remifentanil or fentanyl infusion, at a rate of 0.75, 1.0, or 1.5 microg x kg(-1) x min(-1) after induction of anesthesia with 2% sevoflurane. Middle cerebral artery blood flow velocity was measured by transcranial Doppler (TCD) sonography. Once a baseline set of hemodynamic variables and TCD measurements were recorded, the opioid infusion was started. Measurements were taken at two-minute intervals, starting four minutes prior to laryngoscopy until four minutes following naso-tracheal intubation. RESULTS: Remifentanil caused a more significant decrease in mean arterial pressure and CBFV prior to tracheal intubation than did fentanyl (P < 0.001). During laryngoscopy and for two minutes following tracheal intubation, CBFV increased in all remifentanil groups (P < 0.05), whereas it remained stable in all fentanyl groups. CONCLUSION: This study suggests that fentanyl was more effective than remifentanil at preventing increases in CBFV during and immediately following laryngoscopy and tracheal intubation in children undergoing sevoflurane anesthesia. Fentanyl also seemed to provide a more stable hemodynamic profile prior to laryngoscopy and tracheal intubation when compared to remifentanil.     

麻醉诱导期间咪达唑仑、异丙酚、依托咪酯及硫喷妥钠对脑血流速率的影响

目的 观察不同麻醉药物在麻醉诱导期间对大脑中动脉血流速率的影响.方法 40例病人随机分为4组(每组10例),麻醉诱导药物分别为咪达唑仑0.15mg/kg、异丙酚2mg/kg、依托咪酯0.3mg/kg和硫喷妥钠5mg/kg.给药3min后行气管内插管.麻醉维持采用1%七氟醚-66%氧化亚氮和氧气吸入,同时机械通气维持PETCO2在35～40mmHg.采用经颅多普勒监测仪(TCD),分别于诱导前和诱导1、2、3、5、10、15min测定大脑中动脉血流速率(V-MCA),同时记录动脉血压、心率及PETCO2.结果 给药后1min,异丙酚、依托咪酯和硫喷妥钠可使V-MCA明显降低(P＜0.05),而咪达唑仑组无显著变化(P＞0.05).气管插管后,4组病人的Vm-MCA,其中仅咪达唑仑组与基础值相比有显著差异(P＜0.05),而其他3组与基础值相比无统计学差异(P＞0.05).结论 对于非神经外科手术病人,诱导剂量的异丙酚、依托咪酯和硫喷妥钠对V-MCA的有一定程度的影响,而咪达唑仑影响较小;在对气管插管引起的脑血流速率波动的抑制方面咪达唑仑则作用较弱.     

Differential effects of hyperventilation on cerebral blood flow velocity after tourniquet deflation during sevoflurane, isoflurane, or propofol anesthesia

The purpose of this study was to compare the degree of increase in middle cerebral artery (MCA) blood flow velocity after tourniquet deflation when modulating hyperventilation during orthopedic surgery under sevoflurane, isoflurane, or propofol anesthesia. Twenty-four patients undergoing elective orthopedic surgery were randomly divided into sevoflurane, isoflurane, and propofol groups. Anesthesia was maintained with sevoflurane, isoflurane, or propofol administration with 33% oxygen and 67% nitrous oxide at anesthetic drug concentrations adequate to maintain bispectral values between 45 and 50. A 2.0-MHz transcranial Doppler probe was attached to the patient’s head at the temporal window, and mean blood flow velocity in the MCA (V _mca) was continuously measured. The extremity was exsanguinated with an Esmarch bandage, and the pneumatic tourniquet was inflated to a pressure of 450 mmHg. Arterial blood pressure, heart rate, V _mca and arterial blood gases were measured every minute for 10 min after release of the tourniquet in all three groups. Immediately after tourniquet release, the patients’ respiratory rates were increased to tightly maintain end-tidal carbon dioxide (PetCO₂) at 35 mmHg. No change in partial pressure of carbon dioxide in arterial blood (PaCO₂) was observed pre- and posttourniquet deflation in any of the three groups. Increase in V _mca in the isoflurane group was greater than that in the other two groups after tourniquet deflation. In addition, during the study period, no difference in V _mca after tourniquet deflation was observed between the propofol and sevoflurane groups. Hyperventilation could prevent an increase in V _mca in the propofol and sevoflurane groups after tourniquet deflation. However, hyperventilation could not prevent an increase in V _mca in the isoflurane group.     

Awake intubation increases intracranial pressure without affecting cerebral blood flow velocity in infants

Tracheal intubation is frequently required in neonatal anaesthetic practice. Awake intubation is one method of securing the airway and in certain circumstances, for many anaesthetists, can be preferable to intubation following induction of anaesthesia. Previous studies have inferred that the elevation in anterior fontanelle pressure observed during tracheal intubation in neonates was caused by an increase in cerebral blood flow although it was never measured. In this study, direct methods were used to observe changes in the cerebral circulation. Thirteen neonates, ASA I to III (E), aged from 1 to 34 days of age were studied. Patients were randomized to receive either tracheal intubation awake or following induction of anaesthesia with thiopentone 5 mg · kg^{? 1} and succinylcholine 2 mg · kg^?1. Heart rate, systolic arterial blood pressure, anterior fontanelle pressure, cerebral blood flow velocity (using transcranial Doppler sonography) and oxygen saturation were recorded at the following intervals: baseline (not crying), after intravenous atropine 0.02 mg · kg^{? 1}, during laryngoscopy, immediately after insertion of the endotracheal tube, one and five minutes later. The use of atropine masked the cardiovascular responses to intubation. Whereas the change in anterior fontanelle pressure from baseline was different between the groups (P < 0.05), the cerebral blood flow velocity variables were not. The rise in anterior fontanelle pressure seen in the awake group may be attributed to a reduction of the venous outflow from the cranium thereby increasing cerebral blood volume and sub-sequently the intracranial pressure.     

The effect of sevoflurane on cerebral blood flow velocity in children

BACKGROUND: Sevoflurane is a suitable agent for neuroanesthesia in adult patients. In children, cerebrovascular carbon dioxide reactivity is maintained during hypo- and normocapnia under sevoflurane anesthesia. To determine the effects of sevoflurane on middle cerebral artery blood flow velocity (Vmca) in neurologically normal children, Vmca was measured both at different MAC values and at one MAC over a specified time period, using transcranial Doppler sonography. METHODS: Twenty-six healthy children undergoing elective urological surgery were enrolled (16 patients in part I and 10 in part II). In part I of the study anesthesia comprised sevoflurane 0.5, 1.0 and 1.5 MAC in 30% oxygen and a caudal epidural block. Once steady state had been reached at each sevoflurane MAC level, three measurements of Vmca, mean arterial pressure (MAP) and heart rate (HR) were recorded. In part II of the study patients received sevoflurane 1.0 MAC over a 90-min period, with the same variables being recorded at 15-min intervals. RESULTS: Vmca did not vary significantly at 0.5, 1.0 and 1.5 MAC sevoflurane. There was a significant decrease in MAP between 0.5 MAC and 1.0 MAC sevoflurane (P < 0.005) and also between 1.0 MAC and 1.5 MAC (P < 0.01). There was no significant change in Vmca over 90 min at 1.0 MAC sevoflurane. CONCLUSION: Sevoflurane does not significantly affect cerebral blood flow velocity in healthy children at working concentrations.     

S-ketamine anesthesia increases cerebral blood flow in excess of the metabolic needs in humans

BACKGROUND: Animal studies have demonstrated neuroprotective properties of S-ketamine, but its effects on cerebral blood flow (CBF), metabolic rate of oxygen (CMRO2), and glucose metabolic rate (GMR) have not been comprehensively studied in humans. METHODS: Positron emission tomography was used to quantify CBF and CMRO2 in eight healthy male volunteers awake and during S-ketamine infusion targeted to subanesthetic (150 ng/ml) and anesthetic (1,500-2,000 ng/ml) concentrations. In addition, subjects' GMRs were assessed awake and during anesthesia. Whole brain estimates for cerebral blood volume were obtained using kinetic modeling. RESULTS: The mean +/- SD serum S-ketamine concentration was 159 +/- 21 ng/ml at the subanesthetic and 1,959 +/- 442 ng/ml at the anesthetic levels. The total S-ketamine dose was 10.4 mg/kg. S-ketamine increased heart rate (maximally by 43.5%) and mean blood pressure (maximally by 27.0%) in a concentration-dependent manner (P = 0.001 for both). Subanesthetic S-ketamine increased whole brain CBF by 13.7% (P = 0.035). The greatest regional CBF increase was detected in the anterior cingulate (31.6%; P = 0.010). No changes were detected in CMRO2. Anesthetic S-ketamine increased whole brain CBF by 36.4% (P = 0.006) but had no effect on whole brain CMRO2 or GMR. Regionally, CBF was increased in nearly all brain structures studied (greatest increase in the insula 86.5%; P < 0.001), whereas CMRO2 increased only in the frontal cortex (by 15.7%; P = 0.007) and GMR increased only in the thalamus (by 11.7%; P = 0.010). Cerebral blood volume was increased by 51.9% (P = 0.011) during anesthesia. CONCLUSIONS: S-ketamine-induced CBF increases exceeded the minor changes in CMRO2 and GMR during anesthesia.