Comparison of the hemodynamic effects of sevoflurane anesthesia induction and maintenancevs TIVA in CABG surgery

PURPOSE: To compare the hemodynamic effects of sevoflurane when used for induction and maintenance of anesthesia with a total intravenous technique in patients with known coronary artery disease (CAD). METHODS: Thirty patients undergoing elective coronary artery bypass graft (CABG) were randomly allocated to receive either sevoflurane (S group, n = 15) at a minimal concentration of 4% in oxygen for induction and at 0.5-2 MAC end-tidal concentration for maintenance, or a total intravenous technique (T group, n = 15) consisting of midazolam for induction and propofol for maintenance. In both groups, anesthesia was supplemented with sufentanil and muscle relaxation with cis-atracurium. Hemodynamic measurements included systemic and pulmonary pressures, heart rate, mixed venous oxygen saturation and cardiac output at the following times: pre-induction, 7 and 25 min post-induction, chest closure, one hour after surgery and pre and post tracheal extubation. RESULTS: More patients in the S group (8/15) presented bradycardia in the induction period (T:2/15) (P = 0.05). During maintenance of anesthesia, treatment of hypertension was more frequent in the T group (12/15) than in the S group (6/15) (P = 0.025). All other parameters were comparable. CONCLUSION: Induction of anesthesia in patients with CAD, VCRII with sevoflurane supplemented by sufentanil provided hemodynamic responses comparable with those of TIVA although bradycardia was observed more often with sevoflurane. Intraoperative control of systemic blood pressure was achieved with fewer interventions with a sevoflurane/sufentanil maintenance than with a propofol/sufentanil technique in CABG surgery.     

Dynamic cerebral blood flow autoregulation during sevoflurane anesthesia and TIVA

BACKGROUND: Dynamic cerebral blood flow autoregulation during sevoflurane anesthesia and total intravenous anesthesia (TIVA) is unclear. We examined the cerebral circulation autoregulation during anesthesia by sevoflurane or TIVA. METHODS: We measured mean blood pressure (MBP) and blood flow velocity of the middle cerebral artery by a transcranial Doppler ultrasonography before and during anesthesia using sevoflurane (volatile induction and maintenance of anesthesia (VIMA) group) and using propofol and fentanyl (TIVA group), and the relationship between changes in MBP and cerebral blood flow velocity was evaluated using the method of transfer function analysis. We calculated transfer gain and coherence by cross-spectrum from autospectra of MBP and cerebral blood flow velocity. RESULTS: Transfer gain during anesthesia by TIVA in the low frequency range and high frequency range was near 1 cm.sec-1.mmHg-1. It was about equal to the value of transfer gain before anesthesia. But transfer gain during anesthesia by VIMA was above 2 cm.sec-1.mmHg-1. CONCLUSION: These results suggest that TIVA by propofol and fentanyl maintains the dynamic autoregulation of cerebral blood flow, but sevoflurane impairs the autoregulation.     

Pour ou contre les halogénés en neuroanesthésie pour chirurgie intracrânienne

Isoflurane, desflurane and sevoflurane all preserve cerebrovascular carbone dioxide (CO₂) reactivity. They are all concentration-dependant cerebral vasodilatators and decrease cerebral metabolism. Sevoflurane induces the smallest cerebral vasodilatation and preserve cerebral autoregulation up to 1.5 CAM, compared to isoflurane and desflurane which impair it upon 1 CAM. Propofol has been compared to inhaled agents. Propofol preserve cerebrovascular CO₂ reactivity, blood flow-metabolism coupling, cerebral autoregulation and has no vasodilatation effect. None of the three inhaled agents induce any clinical relevant increase of intracranial pressure (ICP), but studies were conducted in patients without any intracranial hypertension (ICHT). However, compared to propofol, ICP and brain swelling were higher with inhaled agents, more with isoflurane compared to sevoflurane. Finally, neuroprotective properties have been described in experimental model for all the inhaled agents but clinical proofs are still lacking. In conclusion, for intracranial surgery without any ICHT inhaled agents can be used as a maintenance anesthetic with a preference for sevoflurane. In case of ICHT or a risk of ICHT during the surgery, propofol is preferred for it slightest effect on ICP and cerebral hemodynamic.     

Newer inhalation anaesthetics and neuro-anaesthesia: what is the place for sevoflurane or desflurane?

The effects on cerebral circulation and metabolism of sevoflurane and desflurane are largely comparable to isoflurane. Both induce a direct vasodilation of the cerebral vessels, resulting in a less pronounced decrease in cerebral blood flow compared to the decrease in cerebral metabolism. This direct vasodilation seems to be dose-dependent and more pronounced for desflurane > isoflurane > sevoflurane. Many reports suggest luxury perfusion at high concentrations of desflurane. Sevoflurane maintains intact cerebral autoregulation up to 1.5 MAC. Desflurane induces a significant impairment in autoregulation, with a completely abolished autoregulation at 1.5 MAC. Both sevoflurane and desflurane (up to 1.5 MAC) maintain normal CO(2) regulation. As to their effect on final intracranial pressure (ICP), both sevoflurane and desflurane revealed no increases in ICP. However, compared to intravenous hypnotics, subdural ICP is higher with volatiles because of their tendency to increase cerebral swelling after dura opening (isoflurane > sevoflurane). Several case reports have noted seizure-like movements, as well as EEG recorded seizures during induction of sevoflurane anesthesia. Especially, in children during inhalational induction with hyperventilation at a high sevoflurane concentration, severe epileptiform EEG with a hyperdynamic response were observed, which urges for caution using inhalational sevoflurane induction in children for neurosurgical procedures. Neuroprotective properties (reduced neuronal death either by necrosis or apoptosis) have been attributed to all volatile agents. However, these neuroprotective effects have been described in experimental or animal models, so their possible effect on humans remains to be proven.     

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.     

Kardiovaskuläre Effekte von Sevofluran

The cardiovascular effects of sevoflurane are similar to those of isoflurane with some minor exceptions. In contrast to isoflurane and particularly to desflurane, sevoflurane has not been associated with increases in heart rate in healthy volunteers and in patients. The coronary vasodilatory potency of sevoflurane appears to be lower than that of isoflurane and it has not been associated with a reduction of blood flow to collateral myocardium in dogs with steal-prone anatomy. In several multi-center studies of patients with coronary artery disease or at high risk for coronary artery disease receiving either sevoflurane or isoflurane for either cardiac or non-cardiac surgery, the incidence of myocardial ischemia and infarction did not differ between treatment groups. In both human and animal models, sevoflurane preserves cerebral blood flow and reduces cerebral metabolic rate, much like isoflurane.     

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.     

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.     

Sevoflurane, but not propofol, significantly prolongs the Q-T interval

Prolongation of the Q-T interval may be associated with polymorphic ventricular tachycardia known as torsade de pointes, syncope and sudden death. Existing data show that isoflurane prolongs the Q-T interval, whereas halothane shortens it. The aim of this study was to determine whether sevoflurane or propofol affects the Q-T interval. Thirty female patients undergoing gynecologic surgery were randomly assigned to two groups, one receiving inhaled induction with sevoflurane and the other receiving total IV anesthesia with propofol. Before and 20 min after the induction, a six-lead electrocardiogram was recorded, and blood pressure was measured. The Q-T interval and heart rate adjusted Q-T interval (Q-Tc interval) were significantly prolonged during the administration of anesthesia with sevoflurane, while the Q-T interval was significantly shortened, and the Q-Tc interval was statistically unaffected during propofol anesthesia administration. We conclude that, in otherwise healthy female patients, sevoflurane prolongs the Q-Tc. IMPLICATIONS: In this study, we evaluated the effect of sevoflurane induction and anesthesia versus propofol induction and anesthesia on the Q-T interval. Sevoflurane significantly prolonged the Q-T interval and the heart rate adjusted Q-T interval, whereas propofol shortened the Q-T interval but not the heart rate adjusted Q-T interval.     

The effects of sevoflurane and nitrous oxide on middle cerebral artery blood flow velocity and transient hyperemic response.

We studied the effects of sevoflurane, with and without nitrous oxide, on the indices of cerebral autoregulation (transient hyperemic response ratio and the strength of autoregulation) derived from the transient hyperemic response (THR) test. Twelve patients (ASA physical status I or II) aged 18-40 yr presenting for routine non-neurosurgical procedures were recruited. The middle cerebral artery blood flow velocity was continuously recorded using transcranial Doppler ultrasonography. Preinduction THR tests were performed before the patients were anesthetized with alfentanil, propofol, and vecuronium. End-tidal carbon dioxide concentration and mean arterial pressure (to within 10% with a phenylephrine infusion) were maintained at their preinduction values. THR tests were performed sequentially at the following end-tidal sevoflurane concentrations: 2.2% in oxygen, 3.4% in oxygen, 3.4% with 50% nitrous oxide in oxygen, and 2.2% with 50% nitrous oxide in oxygen. Neither 2.2% nor 3.4% sevoflurane significantly affected cerebral autoregulation. The addition of 50% nitrous oxide to the 2.2%, but not the 3.4%, concentration of sevoflurane increased middle cerebral artery blood flow velocity and decreased autoregulatory indices significantly. IMPLICATIONS: Transient hyperemic response is preserved during sevoflurane anesthesia but is significantly impaired when nitrous oxide is added to the lower concentration of sevoflurane (2.2%). These findings have implications for neurosurgical patients undergoing general anesthesia.     

地氟醚复合吗啡快通道麻醉在腹腔镜胆囊切除术的应用

目的 研究地氟醚复合吗啡快通道麻醉在腹腔镜胆囊切除术（LC） 的应用.方法 选择ASAⅠ-Ⅱ级LC 患者90 例,随机分为3 组：P 组（丙泊酚＋ 瑞芬太尼）、S 组（七氟醚＋瑞芬太尼）和D 组（地氟醚＋ 吗啡）,术前和诱导用药相同,麻醉维持：P 组静脉输注丙泊酚、瑞芬太尼和顺式阿曲库铵;S 组吸入七氟醚及静脉输注瑞芬太尼,不追加顺式阿曲库铵;D 组吸入地氟醚及静脉注射吗啡,不追加顺式阿曲库铵.术中观察血流动力学波动情况和呼吸恢复、拔管、离室时间、术中知晓发生率以及苏醒期躁动评分.结果 与P 组比较,D 组和S 组的血压和心率波动例数减少（P 〈 0.05）;与P 组和S 组比较,D 组呼吸恢复、拔管、离室的时间缩短（P 〈 0.05）,苏醒期躁动的评分较高（P 〈 0.05）.3 组患者均未出现术中知晓.结论 地氟醚复合吗啡快通道麻醉应用于腹腔镜胆囊切除术对血流动力学波动影响小,术后苏醒速度快、质量高.     

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.     

Recovery of cognitive function after remifentanil-propofol anesthesia: a comparison with desflurane and sevoflurane anesthesia

We compared the recovery characteristics of remifentanil, desflurane, and sevoflurane when used for anesthesia in elective operative procedures. Sixty ASA physical status I and II patients, aged 18-65 yr, were randomly assigned to receive remifentanil-propofol, desflurane-N2O, or sevoflurane-N2O anesthesia. Before the induction of anesthesia, the patients of the desflurane and sevoflurane groups received fentanyl 2 microg/kg. In all groups, anesthesia was induced with propofol and maintained either with remifentanil 0.25 microg x kg(-1) x min(-1), desflurane, or sevoflurane 0.85 MAC with 65% nitrous oxide in oxygen. Anesthetics were titrated to achieve an adequate level of surgical anesthesia and to maintain mean arterial pressure within 20% of baseline values. Early recovery times and a modified Aldrete Recovery Score > 9 were recorded. Trieger Dot Test and Digit Substitution Test (DSST) were performed the day before surgery and in the postanesthesia care unit to evaluate intermediate recovery. The remifentanil-propofol group had a significantly faster emergence than desflurane or sevoflurane, with no difference between both inhaled anesthetics. Thirty min after anesthesia administration, patients in the remifentanil-propofol and in the desflurane groups gave significantly more correct responses in the DSST compared with sevoflurane (remifentanil 87%, desflurane 83%, sevoflurane 56%), the impairment in the sevoflurane patients corresponding to the effects of a blood alcohol level of approximately 0.1% and, thus, being of clinical importance. Ninety minutes after anesthesia administration, no significant difference could be demonstrated among the groups in the DSST scores. Emergence and return of cognitive function was significantly faster after remifentanil-propofol compared with desflurane and sevoflurane up to 60 min after anesthesia administration. IMPLICATIONS: We compared awakening and intermediate recovery times after remifentanil-propofol anesthesia to desflurane-N2O and sevoflurane-N2O anesthesia. Emergence and return of cognitive function was significantly faster after remifentanil-propofol compared with desflurane and sevoflurane up to 60 min after anesthesia administration.     

Emergence and recovery characteristics of desflurane versus sevoflurane in morbidly obese adult surgical patients: a prospective, randomized study

We compared postoperative recovery after desflurane (n = 25) versus sevoflurane (n = 25) anesthesia in morbidly obese adults (body mass index >/=35) who underwent gastrointestinal bypass surgery via an open laparotomy. After premedication with midazolam and metoclopramide 1 h before surgery, epidural catheter placement, induction of anesthesia with fentanyl and propofol, and tracheal intubation facilitated with succinylcholine, anesthesia was maintained with age-adjusted 1 minimum alveolar concentration (MAC) desflurane or sevoflurane. Fentanyl IV, morphine or local anesthetics epidurally, and vasoactive drugs as needed were used to maintain arterial blood pressure at +/-20% of baseline value and to keep bispectral index of the electroencephalogram values between 40 to 60 U. Although patients were anesthetized with desflurane for a longer time (261 +/- 50 min versus 234 +/- 37 min, mean +/- sd; P < 0.05, desflurane versus sevoflurane, respectively) and for more MAC-hours (4.2 +/- 0.9 h versus 3.7 +/- 0.8 h; P < 0.05), significantly earlier recovery of response to command and tracheal extubation occurred in patients given desflurane than in patients given sevoflurane. The modified Aldrete score was greater in desflurane-anesthetized patients on admission to the postanesthesia care unit (PACU) (P = 0.01) but not at discharge (P = 0.47). On admission to PACU, patients given desflurane had higher oxygen saturations (97.0% +/- 2.4%) than patients given sevoflurane (94.8% +/- 4.4%, P = 0.035). Overall, the incidence of postoperative nausea and vomiting and the use of antiemetics did not differ between the two anesthetic groups. We conclude that morbidly obese adult patients who underwent major abdominal surgery in a prospective, randomized study awoke significantly faster after desflurane than after sevoflurane anesthesia and the patients anesthetized with desflurane had higher oxygen saturation on entry to the PACU.     

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.     

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.     

Inhalational techniques in ambulatory anesthesia

In the current health care environment, anesthesia practitioners are frequently required to reevaluate their practice to be more efficient and cost-effective. Although IV induction with propofol and inhalational induction with sevoflurane are both suitable techniques for outpatients, patients prefer IV induction. Maintenance of anesthesia with the newer inhaled anesthetics (ie, desflurane and sevoflurane) provide for a rapid early recovery as compared with infusion of propofol (ie, TIVA), while allowing easy titratability of anesthetic depth. Titration of hypnotic sedatives using BIS monitoring may reduce the time to awakening and thereby may facilitate fast tracking (ie, bypassing the PACU) and reduce hospital stay. Inhalational anesthesia is associated with a higher incidence of PONV, but no differences have been demonstrated with respect to late recovery (eg, PACU stay and home readiness). Although clinical differences between desflurane and sevoflurane appear to be small, desflurane may be associated with faster emergence, particularly in elderly and morbidly obese patients. Balanced anesthesia with IV propofol induction and inhalation anesthesia with N2O for maintenance, and an LMA for airway management, may be an optimal technique for ambulatory surgery. Inhalational anesthesia may have an economic advantage over a TIVA technique.     

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.     

Propofol anesthesia enhances the pressor response to intravenous ephedrine

The induction of anesthesia with propofol is often associated with a decrease in arterial blood pressure (BP). Although vasopressors are sometimes required to reverse the propofol-induced hypotension, little is known about the effect of propofol on these drugs. We studied the effects of propofol and sevoflurane on pressor response to i.v. ephedrine. Thirty adult patients were randomly assigned to one of two groups. In the Propofol group (n = 15), patients received propofol 2.5 mg/kg i.v. for induction followed by 100 microg x kg(-1) x min(-1) i.v. for maintenance. In the Sevoflurane group (n = 15), anesthesia was induced with sevoflurane 3%-4% in oxygen and maintained with sevoflurane 2% in oxygen. All patients in both groups received ephedrine 0.1 mg/kg i.v. before and after the anesthetic induction. Ephedrine increased the heart rate significantly (P < 0.05) in awake patients in both study groups. In contrast, there was no increase in heart rate after the ephedrine administration under propofol or sevoflurane anesthesia. In awake patients, transient increases in mean BP were observed after i.v. ephedrine in both groups. In the Propofol group, 2 min after the administration of ephedrine, mean BP increased 16% +/- 10% under anesthesia but increased only 4% +/- 6% when the same patients were awake. The magnitudes of the pressor responses to ephedrine during propofol anesthesia were significantly greater (P < 0.05) than during the awake state. However, ephedrine 0.1 mg/kg i.v. showed no significant increases in BP during sevoflurane anesthesia. We conclude that propofol, not sevoflurane, anesthesia augments the pressor responses to i.v. ephedrine. IMPLICATIONS: The effect of anesthetics on vasopressor-mediated cardiovascular effects is poorly understood. We evaluated the pressor response to ephedrine during propofol or sevoflurane anesthesia. Our study suggests that anesthesia-induced hypotension may be easier to reverse with ephedrine during propofol anesthesia than during sevoflurane anesthesia.     

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.