S(+)-ketamine/propofol maintain dynamic cerebrovascular autoregulation in humans

PURPOSE: This study investigates the effects of S(+)-ketamine and propofol in comparison to sevoflurane on dynamic cerebrovascular autoregulation in humans. METHODS: Twenty-four patients were randomly assigned to one of the following anesthetic protocols: group I (n=12): 2.5 mg.kg(-1)*hr(-1) S(+)-ketamine, 1.5-2.5 microg*mL(-1) propofol-target plasma concentration; group II (n=12): 2.0 MAC (4.0 %) sevoflurane. Patients were intubated and ventilated with O(2)/air (PaO(2)=0.33). Following 40 min of equilibration dynamic cerebrovascular autoregulation was measured and expressed as the autoregulatory index (ARI), describing the duration of cerebral hemodynamic recovery in relation to changes in mean arterial blood pressure. Statistics: Mann-Whitney U test (statistical significance was assumed when P <0.05). RESULTS: Dynamic cerebrovascular autoregulation was intact in all patients with S(+)-ketamine/propofol anesthesia as indicated by an ARI of 5.4 +/- 1.1. In contrast, dynamic cerebrovascular autoregulation was significantly delayed with 2.0 MAC sevoflurane (ARI=2.6 +/- 0.7) CONCLUSION: Dynamic cerebrovascular autoregulation is maintained with S(+)-ketamine/propofol-based total iv anesthesia. In contrast, 2.0 MAC sevoflurane delayed dynamic cerebrovascular autoregulation. This supports the use of S(+)-ketamine in combination with propofol in neurosurgical patients based on its neuroprotective potential along with maintained cerebrovascular physiology.     

Cerebral autoregulation in awake versus isoflurane-anesthetized rats

We evaluated regional cerebral and spinal cord blood flow in rats during isoflurane anesthesia. Tissue blood flow was measured in cerebral cortex, subcortex, midbrain, and spinal cord using radioactive microspheres. Blood flow autoregulation was measured within the following arterial blood pressure ranges (mm Hg): 1 = less than 50, 2 = 50-90, 3 = 90-130, 4 = 130-170, 5 = greater than 170. Arterial blood pressure was increased using phenylephrine infusion and decreased with ganglionic blockade and hemorrhage. Three treatment groups were studied: 1 = awake control, 2 = 1.0 minimum alveolar anesthetic concentration (MAC) isoflurane, 3 = 2.0 MAC isoflurane. Autoregulation was seen in awake rats from 50 to 170 mm Hg in all tissues. The autoregulatory coefficient (change in blood flow/change in blood pressure) was increased in midbrain and spinal cord during 1.0 MAC isoflurane and in all tissues during 2.0 MAC isoflurane (P less than 0.05). Within the arterial blood pressure range of 90-130 mm Hg, isoflurane produced the following changes in tissue blood flow (percent of awake control): 1.0 MAC isoflurane: cortex = 87% +/- 8% (P greater than 0.30), subcortex = 124% +/- 11% (P greater than 0.05), midbrain = 263% +/- 20% (P less than 0.001), spinal cord = 278% +/- 19% (P less than 0.001); 2.0 MAC isoflurane: cortex = 137% +/- 13% (P less than 0.05), subcortex = 272% +/- 24% (P less than 0.001), midbrain = 510% +/- 53% (P less than 0.001), spinal cord = 535% +/- 50% (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Sevoflurane increases lumbar cerebrospinal fluid pressure in normocapnic patients undergoing transsphenoidal hypophysectomy.

BACKGROUND: The data on the effect of sevoflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that sevoflurane would increase intracranial pressure as compared to propofoL METHODS: In 20 patients with no evidence of mass effect undergoing transsphenoidal hypophysectomy, anesthesia was induced with intravenous fentanyl and propofol and maintained with 70% nitrous oxide in oxygen and a continuous propofol infusion, 100 microg x kg(-1) x min(-1). The authors assigned patients to two groups randomized to receive only continued propofol infusion (n = 10) or sevoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the sevoflurane group received, in random order, two concentrations (0.5 times the minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of sevoflurane for 10 min each. The authors continuously monitored lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations. RESULTS: Lumbar CSF pressure increased by 2+/-2 mmHg (mean+/-SD) with both 0.5 MAC and 1 MAC of sevoflurane. Cerebral perfusion pressure decreased by 11+/-5 mmHg with 0.5 MAC and by 15+/-4 mmHg with 1.0 MAC of sevoflurane. Systolic blood pressure decreased with both concentrations of sevoflurane. To maintain blood pressure within predetermined limits (within+/-20% of baseline value), phenylephrine was administered to 5 of 10 patients in the sevoflurane group (range = 50-300 microg) and no patients in the propofol group. Lumbar CSF pressure, cerebral perfusion pressure, and systolic blood pressure did not change in the propofol group. CONCLUSIONS: Sevoflurane, at 0.5 and 1.0 MAC, increases lumbar CSF pressure. The changes produced by 1.0 MAC sevoflurane did not differ from those observed in a previous study with 1.0 MAC isoflurane or desflurane.     

Fast-tracking after immersion lithotripsy: general anesthesia versus monitored anesthesia care

Both monitored anesthesia care (MAC) and general anesthesia (GA) offer advantages over epidural anesthesia for immersion lithotripsy. We compared propofol-based MAC and desflurane-based GA techniques for outpatient lithotripsy. After receiving midazolam 2 mg IV, 100 subjects were randomly assigned to one of two anesthetic treatment groups. In the MAC group, propofol 50-100 microg. kg(-1). min(-1) IV was titrated to maintain an observer's assessment of alertness/sedation score of 2-3 (5 = awake/alert to 1 = asleep). Remifentanil 0.05 microg.kg(-1). min(-1) IV supplemented with 0.125 microg/kg IV boluses, was administered for pain control. In the GA group, anesthesia was induced with propofol 1.5 mg/kg IV and remifentanil 0.125 microg/kg IV and maintained with desflurane (2%-4% inspired) and nitrous oxide (60%). Tachypnea (respiratory rate >20 breaths/min) was treated with remifentanil 0.125 microg/kg IV boluses. In the GA group, droperidol (0.625 mg IV) was administered as a prophylactic antiemetic. Recovery times and postoperative side effects were assessed up to 24 h after the procedure. Compared with MAC, the use of GA reduced the opioid requirement and decreased movements and episodes of desaturation (<90%) during the procedure. Although the GA group took longer to return to an observer's assessment of alertness/sedation score of 5, discharge times were similar in both groups. We conclude that GA can provide better conditions for outpatient immersion lithotripsy than MAC sedation without delaying discharge. IMPLICATIONS: A desflurane-based general anesthetic technique using the cuffed oropharyngeal airway device was found to be a highly acceptable alternative to propofol-based monitored anesthesia care sedation for outpatient immersion lithotripsy.     

Cerebral autoregulation and CO2 reactivity in anterior and posterior cerebral circulation during sevoflurane anesthesia

The purpose of the study was to compare cerebral autoregulation (CA) and CO2 reactivity (CO2R) between the anterior and posterior circulation under sevoflurane anesthesia. We studied 9 adult ASA physical status I patients (22-47 yr) scheduled for elective orthopedic surgery. Blood flow velocity in the middle cerebral artery (Vmca) and in the basilar artery (Vba) were measured using transcranial Doppler ultrasonography. For CA testing, arterial blood pressure was increased using phenylephrine infusion. CA was quantified with the autoregulatory index (ARI). CO2R was investigated at PaCO2 of 30 +/- 2.8 mm Hg, 39.4 +/- 2.6 mm Hg, and 48.7 +/- 2.8 mm Hg. Linear regression analysis was used for CO2R. We found ARI was preserved in both arteries: ARImca (middle cerebral artery) = 0.72 +/- 0.2; ARIba (basilar artery) = 0.66 +/- 0.2; P = 0.5. With regard to CO2R, Vmca increased with slope of 1.7 cm/s/mm Hg PaCO2, Vba increased with slope of 1.5 cm/s/mm Hg PaCO2; P = 0.83. Absolute Vmca was higher compared with Vba; P < 0.05. We conclude that in healthy individuals under 0.5 MAC of sevoflurane and small-dose remifentanil: 1) mean flow velocities of BA are less than those of MCA; 2) autoregulation and CO2R are preserved in the basilar artery and are similar to those of MCA.     

Remifentanil administration during monitored anesthesia care: are intermittent boluses an effective alternative to a continuous infusion?

This randomized, double-blind study was designed to evaluate the analgesic effectiveness and respiratory stability of remifentanil when administered as intermittent bolus injections, a variable-rate infusion, or a combination of a constant basal infusion supplemented with intermittent boluses during monitored anesthesia care (MAC). Forty-five patients undergoing extracorporeal shock wave lithotripsy (ESWL) procedures were randomly assigned to one of the three modes of remifentanil administration. All patients received midazolam 2 mg i.v., followed by a propofol infusion at 50 microg x kg(-1) x min(-1). Two minutes before administering a series of test shock waves: Group I received a remifentanil infusion of 0.1 microg x kg(-1) x min(-1), and a saline bolus (5 mL); Group II received a saline infusion and a remifentanil bolus (25 microg in 5 mL); and Group III received a remifentanil infusion of 0.05 microg x kg(-1) x min(-1), and a remifentanil bolus (12.5 microg in 5 mL). The average pain intensity was scored on an 11-point scale, with 0 = no pain to 10 = severe pain. During the ESWL procedure, pain was treated by increasing the study drug infusion rate by 25%-50% and administering 5-mL bolus injections of the study medication in Groups I (saline) and II (remifentanil 25 microg). In Group III, intermittent 5-mL boluses (remifentanil 12.5 microg) were administered as needed. Patients in Groups II and III reported lower pain scores in response to the test shocks. Significantly more remifentanil was administered in Group I (379 +/- 207 microg) than in Group II (201 +/- 136 microg). However, more interventions were required for the treatment of intraoperative pain in the intermittent bolus group (Group II). When remifentanil is administered as the analgesic component of a MAC technique, these data support the use of intermittent bolus doses (12.5-25 microg) alone or in combination with a basal infusion (0.05 microg x kg(-1) x min(-1)) as alternatives to a variable-rate continuous infusion. IMPLICATIONS: In this study, three different modes of remifentanil administration were used during monitored anesthesia care for extracorporeal shock wave lithotripsy procedures. These results suggest that using intermittent bolus injections of remifentanil (25 microg) or a continuous infusion (0.05 microg x kg(-1) x min(-1)) supplemented with intermittent bolus (12.5 microg) injections may be more effective than a variable-rate infusion of remifentanil during propofol sedation.     

Total intravenous anesthesia with remifentanil, propofol and cisatracurium in end-stage renal failure

PURPOSE: To compare recovery parameters of total intravenous anesthesia (TIVA) with remifentanil and propofol, hemodynamic responses to perioperative events, and pharmacodynamic parameters of cisatracurium in 22 end-stage renal failure and 22 normal renal function patients. METHODS: Anesthesia was induced with 2-3 mg x kg(-1) propofol and 1 microg x kg(-1) remifentanil and maintained with 75 microg x kg(-1) x min(-1) propofol and propofol initial infusion of 0.2 microg x kg(-1) x min(-1) propofol. Arterial pressure and heart rate were maintained by remifentanil infusion rate adjustments. The first twitch (T1) was maintained at 25% by an infusion of cisatracurium. RESULTS: There was no difference in the time to maintenance of adequate respiration, date of birth recollection, first analgesic administration, between the renal failure (4.8+/-2.5, 7.8+/-3.2, 12.3+/-5.3 min respectively) and the control group (5.2+/-2.8, 8.1+/-3.1, 12.7+/-5.5 min): nor were there any differences in the time to 25% T1 recovery, T1 recovery from 25% to 75%, or cisatracurium infusion rate between the renal failure group (32.1 +/-10.8 min, 18.2+/-5.5 min, 0.89+/-0.29 microg x kg(-1) min(-1) respectively) and the control group (35.9 (7.9 min, 18.4+/-3.8 min, 0.95+/-0.22 microg x kg(-1) x min(-1)). CONCLUSION: End-stage renal failure does not prolong recovery from TIVA with remifentanil and propofol, or the recovery from cisatracurium neuromuscular block.     

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.     

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.     

An investigation of monoamine receptors involved in antinociceptive effects of antidepressants

In this prospective study, we evaluated the effects of remifentanil in ASA I-II patients undergoing transsphenoidal surgery. After the induction of anesthesia, patients were randomly allocated to the Isoflurane (n = 22, 60% nitrous oxide, isoflurane up to 2% end-tidal) or Remifentanil group (n = 21, 60% nitrous oxide, 0.5% end-tidal isoflurane, remifentanil up to 2 microg x kg(-1) x min(-1)). If mean arterial pressure (MAP) increased >80 mm Hg during maximal dosage of isoflurane or remifentanil, labetalol was administered. At the end of anesthesia, extubation and awakening times, respiratory rate, SpO(2), MAP, heart rate, and adverse effects were recorded. Hemodynamics and bleeding (minimal, mild, moderate, severe) were not different between groups. Bleeding grade increased with MAP >80 mm Hg (P < 0.001). Labetalol was administered to 20 patients in the Isoflurane group, and 10 patients in the Remifentanil group (P < 0.01). The dose of labetalol was larger in the Isoflurane group (1.0 +/- 0.6 versus 0.5 +/- 0.7 mg/kg, P < 0.05). Time to extubation did not differ, whereas time to follow commands was shorter in Remifentanil patients (16 +/- 8 versus 10 +/- 2 min, P < 0.01). No adverse effects occurred in the early postoperative period. IMPLICATIONS: In patients undergoing transsphenoidal surgery, balanced anesthesia with remifentanil (0.22 +/- 0.17 microg x kg(-1) x min(-1)) provides faster awakening time, as compared with large-dose volatile-based anesthesia, without the risk of postoperative opioid respiratory depression.     

The effect of hypocapnia on the autoregulation of cerebral blood flow during administration of isoflurane

Isoflurane impairs autoregulation of cerebral blood flow in a dose-related manner. Previous investigations in several other conditions have demonstrated that impaired autoregulation can be restored by hyperventilation. We hypothesized that hypocapnia may restore cerebral autoregulation impaired by isoflurane anesthesia. We administered isoflurane in 100% oxygen to 12 healthy patients aged 21-59 yr scheduled for elective nonneurological surgery. Isoflurane end-tidal concentration was individualized at 0.1% to 0.2% less than that required to induce short periods of isoelectric electroencephalogram. This resulted in an end-tidal isoflurane concentration of 1.6% +/- 0.2% (mean +/- sd) corresponding to an age-adjusted minimum alveolar anesthetic concentration multiple of 1.4. Mean arterial blood pressure was reduced to <80 mm Hg, by infusion of remifentanil if required. Cerebral autoregulation was assessed by infusing phenylephrine to increase mean arterial blood pressure to 100 mm Hg while monitoring middle cerebral artery blood flow velocity with transcranial Doppler ultrasonography. The change in flow velocity was used to calculate the autoregulation index (ARI). The ARI ranges between 0 and 1 and an ARI < or =0.4 indicates significantly impaired autoregulation. Autoregulation was tested twice in randomized order: once during normocapnia (Paco(2) 38-43 mm Hg) and once during hypocapnia (Paco(2) 27-34 mm Hg). The median (interquartile range) ARI was 0.29 (0.23-0.64) during normocapnia and 0.77 (0.70-0.78) during hypocapnia (P < 0.005). Of the 12 subjects, autoregulation was significantly impaired in 8 subjects during normocapnia and none during hypocapnia (P = 0.001). Hypocapnia restored cerebral autoregulation in normal subjects during isoflurane-induced impairment of autoregulation.     

Isoflurane and Sevoflurane Anesthesia in Pigs with a Preexistent Gas Exchange Defect

Background : Decreased arterial partial pressure of oxygen (Pao2) during volatile anesthesia is well-known. Halothane has been examined with the multiple inert gas elimination technique and has been shown to alter the distribution of pulmonary blood flow and thus Pao2. The effects of isoflurane and sevoflurane on pulmonary gas exchange remain unknown. The authors hypothesized that sevoflurane with a relatively high minimum alveolar concentration (MAC) would result in significantly more gas exchange disturbances in comparison with isoflurane or control.

Methods : This study was performed in a porcine model with an air pneumoperitoneum that generates a reproducible gas exchange defect. After a baseline measurement of pulmonary gas exchange (multiple inert gas elimination technique) during propofol anesthesia, 21 pigs were randomly assigned to three groups of seven animals each. One group received isoflurane anesthesia, one group received sevoflurane anesthesia, and one group was continued on propofol anesthesia (control). After 30 min of volatile anesthesia at 1 MAC or propofol anesthesia, a second measurement (multiple inert gas elimination technique) was performed.

Results : At the second measurement, inert gas shunt was 15 +/- 3% (mean +/- SD) during sevoflurane anesthesia versus 9 +/- 1% during propofol anesthesia (P = 0.02). Blood flow to normal ventilation/perfusion ( A/ ) lung areas was 83 +/- 5% during sevoflurane anesthesia versus 89 +/- 1% during propofol anesthesia (P = 0.04). This resulted in a Pao2 of 88 +/- 11 mmHg during sevoflurane anesthesia versus 102 +/- 15 mmHg during propofol anesthesia (P = 0.04). Inert gas and blood gas variables during isoflurane anesthesia did not differ significantly from those obtained during propofol anesthesia.     

Isoflurane and sevoflurane anesthesia in pigs with a preexistent gas exchange defect.

BACKGROUND: Decreased arterial partial pressure of oxygen (PaO2) during volatile anesthesia is well-known. Halothane has been examined with the multiple inert gas elimination technique and has been shown to alter the distribution of pulmonary blood flow and thus PaO2. The effects of isoflurane and sevoflurane on pulmonary gas exchange remain unknown. The authors hypothesized that sevoflurane with a relatively high minimum alveolar concentration (MAC) would result in significantly more gas exchange disturbances in comparison with isoflurane or control. METHODS: This study was performed in a porcine model with an air pneumoperitoneum that generates a reproducible gas exchange defect. After a baseline measurement of pulmonary gas exchange (multiple inert gas elimination technique) during propofol anesthesia, 21 pigs were randomly assigned to three groups of seven animals each. One group received isoflurane anesthesia, one group received sevoflurane anesthesia, and one group was continued on propofol anesthesia (control). After 30 min of volatile anesthesia at 1 MAC or propofol anesthesia, a second measurement (multiple inert gas elimination technique) was performed. RESULTS: At the second measurement, inert gas shunt was 15 +/- 3% (mean +/- SD) during sevoflurane anesthesia versus 9 +/- 1% during propofol anesthesia (P = 0.02). Blood flow to normal ventilation/perfusion (V(A)/Q) lung areas was 83 +/- 5% during sevoflurane anesthesia versus 89 +/- 1% during propofol anesthesia (P = 0.04). This resulted in a PaO2 of 88 +/- 11 mmHg during sevoflurane anesthesia versus 102 +/- 15 mmHg during propofol anesthesia (P = 0.04). Inert gas and blood gas variables during isoflurane anesthesia did not differ significantly from those obtained during propofol anesthesia. CONCLUSIONS: In pigs with an already existent gas exchange defect, sevoflurane anesthesia but not isoflurane anesthesia causes significantly more gas exchange disturbances than propofol anesthesia does.     

A comparison of anaesthesia using remifentanil combined with either isoflurane, enflurane or propofol in patients undergoing gynaecological laparoscopy, varicose vein or arthroscopic surgery

BACKGROUND: Anaesthesia comprising remifentanil plus isoflurane, enflurane or propofol was randomly evaluated in 285, 285 and 284 patients, respectively, undergoing short-procedure surgery. METHODS: Anaesthesia was induced with propofol (0.5 mg x kg(-1) and 10 mg x 10 s(-1)), and a remifentanil bolus (1 microg x kg(-1)) and infusion at 0.5 microg x g(-1) x min(-1). Five minutes after intubation, remifentanil infusion was halved and 0.5 MAC of isoflurane or enflurane, or propofol at 100 microg x kg(-1) x min(-1) were started and titrated for maintenance. RESULTS: Patient demography and anaesthesia duration were similar between the groups. Surgery was performed as daycases (52%) or inpatients (48%). The median times (5-7 min) to extubation and postoperative recovery were similar between the groups. Responses to tracheal intubation (15% vs 8%) and skin incision (13% vs 7%) were significantly greater in the total intravenous anaesthesia (TIVA) group (P<0.05). Fewer patients given remifentanil and isoflurane (21%) or enflurane (19%) experienced > or =1 intraoperative stress response compared to the TIVA group (28%) (P<0.05). Median times to qualification for and actual recovery room discharge were 0.5-0.6 h and 1.1-1.2 h, respectively. The most common remifentanil-related symptoms were muscle rigidity (6-7%) at induction, hypotension (3-5%) and bradycardia (1-4%) intraoperatively and, shivering (6-7%), nausea and vomiting postoperatively. Nausea (7%) and vomiting (3%) were significantly lower with TIVA compared with inhaled anaesthetic groups (14-15% and 6-8%, respectively; P<0.05). CONCLUSION: Anaesthesia combining remifentanil with volatile hypnotics or TIVA with propofol was effective and well tolerated. Times of extubation, postanaesthesia recovery and recovery room discharge were rapid, consistent and similar for all three regimens.     

Bispectral index-guided administration of anaesthesia: comparison between remifentanil/propofol and remifentanil/isoflurane

BACKGROUND AND OBJECTIVE: The bispectral index of the electroencephalogram is a measure of the hypnotic component of anaesthesia and can be used to guide the administration of anaesthesia. This study compares bispectral index-guided anaesthesia with remifentanil and either propofol or isoflurane. METHODS: Eighty consenting patients were randomly assigned to two groups. Following induction with propofol and remifentanil, anaesthesia was maintained with remifentanil/propofol or remifentanil/isoflurane. Remifentanil infusion rates were guided by haemodynamic responses--maintaining mean arterial pressure and heart rate within 20% of baseline. Propofol and isoflurane administration was guided using the bispectral index (45-60). Thirty minutes before the end of surgery, morphine was administered (0.15 mg kg(-1) intravenously). Fifteen minutes before end of surgery, propofol and isoflurane were reduced (bispectral index 60-75). At the end of surgery, the anaesthetic agents were discontinued. Groups were compared for recovery, remifentanil doses and signs of inadequate anaesthesia using the chi2-test and ANOVA (P < 0.05). RESULTS: The duration of surgery was longer in the propofol/remifentanil group (121 +/- 53 versus 94 +/- 40 min). Recovery data were not different between groups. The remifentanil infusion rate was significantly lower with additional isoflurane (0.18 +/- 0.06 microg kg(-1) min(-1)) than with additional propofol (0.31 +/- 0.20 microg kg(-1) min(-1)). The propofol infusion rate was 123 +/- 48 microg kg(-1) min(-1); isoflurane concentration was 0.66 +/- 0.13%. CONCLUSIONS: Bispectral index-guided anaesthesia with remifentanil plus propofol or isoflurane results in the absence of postoperative recall and a fast recovery with both drug combinations. In our patients, at comparable bispectral index-levels, haemodynamic control requires higher doses of remifentanil with propofol than with isoflurane.     

Desflurane increases cerebral blood flow velocity when used for rapid emergence from propofol anesthesia in children

PURPOSE: Desflurane may be used to replace propofol at the end of anesthesia to facilitate rapid emergence. This study determined the effect of administering desflurane during emergence of anesthesia on middle cerebral artery blood flow velocity (Vmca) in children anesthetized with propofol. METHODS: Thirty healthy children aged one to six years scheduled for orchidopexy or hypospadias repair under general anesthesia were enrolled. Anesthesia was maintained with a propofol infusion targeting an estimated serum level of 3 microg x mL(-1), remifentanil 0.2 microg x kg(-1) x min(-1) and a caudal epidural block. Transcranial Doppler sonography was used to measure Vmca at five-minute intervals. In half the patients, propofol was substituted with desflurane 1 MAC, 30 min prior to the end of the surgical procedure. Once steady-state had been achieved recordings of Vmca, heart rate, and mean arterial pressure were resumed. Upon termination of the surgical procedure, the maintenance agent was discontinued and recordings continued at one-minute intervals during emergence of anesthesia. RESULTS: There were no demographic differences between the two groups. Vmca increased from 37.2 +/- 3.1 cm x sec(-1) to 57.7 +/- 4.1 cm x sec(-1) when propofol was changed to desflurane (P < 0.01). Upon emergence of anesthesia, Vmca decreased from 57.8 +/- 4.2 cm x sec(-1) to 37.8 +/- 3.2 cm x sec(-1) in the desflurane group (P < 0.01) but remained unchanged in the propofol group. CONCLUSION: Desflurane is associated with an increase in cerebral blood flow velocity when used to facilitate rapid emergence following a propofol infusion in children. This may be of clinical significance in patients with intracranial pathology.     

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

The purpose of this study was to measure and compare the relationship of cardiovascular depression and dose during equal potent levels of halothane and isoflurane anesthesia in neonates (n = 19) (16.7 +/- 6.9 days) and infants (n = 54) (6.1 +/- 3.1 mo). Seventy-three children had heart rate, arterial blood pressure, and pulsed Doppler pulmonary blood flow velocity as well as two-dimensional echocardiographic assessments of left ventricular area and length recorded just before anesthesia induction. Anesthesia was induced by inhalation of increasing inspired concentrations of halothane or isoflurane in oxygen using a pediatric circle system and mask. During controlled ventilation, halothane and isoflurane concentrations were adjusted to maintain 1.0 MAC and then 1.5 MAC (corrected for age), and echocardiographic and hemodynamic measurements were repeated. A final cardiovascular measurement was recorded after intravenous administration of 0.02 mg/kg of atropine. All measurements were completed before tracheal intubation and the start of elective surgery. In neonates, 1.0 MAC concentrations of halothane and isoflurane decreased cardiac output (74% +/- 16%), stroke volume (75% +/- 15%), and ejection fraction (76% +/- 15%) similarly from awake levels. Decreases in cardiac output, stroke volume, and ejection fraction with halothane and isoflurane were significantly larger at 1.5 MAC (approximately 35% decreases from awake values) than at 1.0 MAC. Heart rate decreased significantly during 1.5 MAC halothane anesthesia (94% +/- 4%) but remained unchanged during isoflurane anesthesia. In infants, 1.0 MAC halothane and isoflurane decreased cardiac output (83% +/- 12%), stroke volume (78% +/- 12%), and ejection fraction (74% +/- 12%) when compared with awake measures.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Desflurane reduces the effective therapeutic infusion rate (ETI) of cisatracurium more than isoflurane, sevoflurane, or propofol

PURPOSE: The present study investigated the interaction between the cumulative dose requirements of cisatracurium and anesthesia with isoflurane, sevoflurane, desflurane or propofol using closed-loop feedback control. METHODS: Fifty-six patients (18-85 yr, vitrectomies of more than one hour) were studied. In the volatile anesthetics groups, anesthesia was maintained by 1.3 MAC of isoflurane, sevoflurane or desflurane; in the propofol group, anesthesia was maintained by a continuous infusion of 6-8 mg.kg(-1).hr(-1) propofol. After bolus application of 0.1 mg.kg(-1) cisatracurium, a T1%-level of 10% of control level (train-of-four stimulation every 20 sec) was maintained using closed-loop feedback controlled infusion of cisatracurium. The effective therapeutic infusion rate (ETI) was estimated from the asymptotic steady-state infusion rate Iss. The Iss was derived from fitting an asymptotic line to the measured cumulative dose requirement curve. The ETI of the different groups was compared using Kruskal-Wallis- test, followed by rank sum test, corrected for the number of comparisons, P <0.05 was regarded as showing significant difference. RESULTS: ETI in the isoflurane group was 35.6 +/- 8.6 microg.m(-2).min(-1), in the sevoflurane group 36.4+/- 11.9 microg m(-2).min(-1), in the desflurane group 23.8 +/- 6.3 microg.m(-2).min(-1). The ETI of the volatile anesthetic groups were all significantly lower than the ETI in the propofol group at 61.7 +/- 25.3 microg.m(-2).min(-1) (P <0.002). The ETI in the desflurane group was significantly lower than in all other groups (P <0.02). CONCLUSION: In comparison to propofol, isoflurane, sevoflurane and desflurane reduce the cumulative dose requirements of cisatracurium to maintain a 90% neuromuscular blockade by 42%, 41% and 60%, respectively.     

Comparison of total intravenous anesthesia and sevoflurane-fentanyl anesthesia for outpatient otorhinolaryngeal surgery

STUDY OBJECTIVE: To compare the recovery characteristics of two widely used anesthetic techniques: remifentanyl-propofol and sevoflurane-fentanyl in a standardized ambulatory population.DESIGN: Randomized, single-blinded study. SETTING: University-affiliated medical center. PATIENTS: 50 ASA physical status I and II patients undergoing elective ambulatory otorhinolaryngeal surgery. INTERVENTIONS: Patients were randomized two groups to receive total intravenous anesthesia (TIVA group) with remifentanil and propofol or sevoflurane-fentanyl (SF group). TIVA patients received induction with propofol 1.5 mg/kg intravenously (IV) and remifentanil 0.5 microg/kg IV. The anesthesia was continued with a continuous infusion of propofol 100 microg/kg/min and remifentanil 0.0625-0.25 microg/kg/min. The SF group received, at induction, fentanyl 2 microg/kg followed by propofol 1.5 mg/kg IV. Maintenance was obtained with 1 to 1.5 minimum alveolar concentration of sevoflurane and bolus of fentanyl 1 microg/kg IV as needed. MEASUREMENTS AND MAIN RESULTS: Early recovery times (eye opening, response to commands, extubation, orientation, operating room stay after surgery, and Aldrete score > or =9) and patient satisfaction were similar between the two groups. Postanesthetic discharge scoring system (PADSS) > or = 9 was significantly shorter for the TIVA group (135.9 +/- 51 vs. 103 +/- 32 min) (p < 0.01) but this difference was not associated with a shorter postanesthesia care unit (PACU) length of stay. CONCLUSION: Early recovery times are comparable between total intravenous anesthesia and sevoflurane-based anesthesia. Even though patients in the TIVA group achieved home readiness criteria in a significantly shorter time, this technique does not shorten PACU length of stay, which depends instead on multiple nonmedical and administrative issues.