Pipecuronium-induced neuromuscular blockade during nitrous oxide-fentanyl, enflurane, isoflurane, and halothane anesthesia in surgical patients.

This study was designed to determine the capacity of several anesthetics to augment pipecuronium neuromuscular blockade. The potency of pipecuronium was determined with single-bolus administration of 20-50 micrograms/kg in 160 patients. Patients were anesthetized with N2O/O2 (60:40) supplemented with fentanyl (4-5 micrograms/kg), halothane (0.8%), isoflurane (1.2%), or enflurane (1.7%). Neuromuscular blockade was measured by an acceleration-responsive transducer (the Accelograph, Biometer International, Odense, Denmark). Responses were defined in terms of percent depression in first-twitch height and train-of-four response, and the dose-response curves were constructed after probit transformation of the responses. The dose-response curves were found to be parallel for both first twitch height and train-of-four responses. The dose-response lines for the enflurane and isoflurane groups were displaced significantly (P less than 0.01) to the left of the line for the fentanyl-N2O group. The calculated doses producing 50% depression of first twitch height were 21.9, 21.2, 18.9, and 17.8 micrograms/kg for the N2O-fentanyl, halothane, isoflurane, and enflurane groups, respectively. Corresponding calculated doses for 50% depression of train-of-four response were significantly smaller (15.5, 14.4, 13.7, 11.9 micrograms/kg, respectively). The enhancing effects of the volatile anesthetics were reflected by significant prolongation of the clinical duration of neuromuscular blockade by pipecuronium. It is concluded that the potency of pipecuronium is enhanced more by enflurane and isoflurane than halothane or fentanyl-N2O anesthesia.     

Vecuronium-induced neuromuscular blockade during enflurane, isoflurane, and halothane anesthesia in humans

To determine the effect of the commonly used volatile anesthetics on a vecuronium-induced neuromuscular blockade, the authors studied 54 patients anesthetized with 1.2 MAC or 2.2 MAC enflurane, isoflurane, or halothane (MAC value includes contribution from 60% nitrous oxide). During 1.2 MAC enflurane, isoflurane, and halothane, the ED50S (the doses depressing twitch tension 50%) for vecuronium were 12.8, 14.7, and 16.9 micrograms/kg, respectively. During 2.2 MAC enflurane, isoflurane, and halothane, the ED50S for vecuronium were 6.3, 9.8, and 13.8 micrograms/kg, respectively (P less than 0.05). Time from injection to peak effect was the same for each anesthetic group (6.5 +/- 0.5 min, mean +/- SD), except for the group given 2.2 MAC enflurane (9.7 +/- 0.6 min) (P less than 0.05). The duration of a 50% block from injection to 90% recovery was the same for each group (mean 20 +/- 4 min), except for the group given 2.2 MAC enflurane (46.5 min) (P less than 0.05). The authors conclude that enflurane is the most potent volatile anesthetic, followed by isoflurane and then halothane, in augmenting a vecuronium-induced neuromuscular blockade. Increasing the concentration of volatile anesthetic has less effect on a neuromuscular blockade produced by vecuronium than on one produced by other nondepolarizing relaxants (e.g., pancuronium and d-tubucurarine).     

Recovery from vecuronium neuromuscular blockade following neostigmine administration in infants, children, and adults during halothane anesthesia

To determine whether neostigmine had different effects in pediatric patients during vecuronium neuromuscular blockade, the rate of recovery following neostigmine administration was compared in infants (n = 8), children (n = 10), and adults (n = 10) during nitrous oxide-halothane anesthesia. After induction of anesthesia, patients received 100 micrograms/kg of vecuronium. The EMG response of the adductor pollicis was monitored after train-of-four (TOF) stimulation of the ulnar nerve every 20 s. When the first twitch of TOF spontaneously recovered to 10% of control value, neostigmine was injected (40 micrograms/kg in adults, 30 micrograms/kg in infants and children). During the first few minutes following neostigmine administration, no differences were observed between the three groups. After the 8 min, recovery was more rapid in children than in infants and adults up to and including the 15th min. Ten minutes after neostigmine administration, the first twitch (mean +/- SD) reached 97 +/- 3%, 99 +/- 2%, and 97 +/- 5% of control value in infants, children, and adults, respectively; TOF ratio was greater in children (0.96 +/- 0.03) than in either adults (0.82 +/- 0.17) or in infants (0.83 +/- 0.14) (P less than 0.05). During the first minutes after neostigmine administration, the lack of difference in TOF recovery in the three groups suggests that neostigmine is the main factor of recovery. In contrast, the more complete recovery after the eighth minute in children could be due to the faster rate of spontaneous recovery from vecuronium induced neuromuscular blockade in children.     

The thermoregulatory threshold in humans during nitrous oxide-fentanyl anesthesia

Narcotics and nitrous oxide (N2O) inhibit thermoregulatory responses in animals. The extent to which N2O/fentanyl anesthesia lowers the thermoregulatory threshold in humans was tested by measuring peripheral cutaneous vasoconstriction using skin-surface temperature gradients (forearm temperature-fingertip temperature) and the laser Doppler perfusion index. Fifteen unpremedicated patients were anesthetized with N2O (70%) and fentanyl (10 micrograms/kg iv bolus followed by 4 micrograms.kg-1.h-1 infusion) during elective, donor nephrectomy. Patients were randomly assigned to undergo additional warming (humidified respiratory gases, warmed intravenous fluids, and a heating blanket over the legs; n = 5) or standard temperature management (no special warming measures; n = 10). Significant vasoconstriction was prospectively defined as a skin-surface temperature gradient between forearm surface and finger-tip surface greater than or equal to 4 degrees C, and the thermoregulatory threshold was defined as the esophageal temperature at which such vasoconstriction occurred. Vasoconstriction did not occur in the patients who received additional warming and thus remained nearly normothermic [average minimum esophageal temperature = 35.8 +/- 0.4 degrees C (SD)] but did in six hypothermic patients at a mean esophageal temperature of 34.2 +/- 0.5 degrees C. Four hypothermic patients developed a passive thermal steady state without becoming sufficiently cold to trigger vasoconstriction. Thus, active thermoregulation occurs during N2O/fentanyl anesthesia but does not occur until core temperatures are approximately 2.5 degrees C lower than normal. The thermoregulatory threshold during N2O/fentanyl anesthesia is similar to that previously determined during halothane (34.4 +/- 0.2 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)     

Mivacurium-induced neuromuscular blockade during sevoflurane and halothane anaesthesia in children

The neuromuscular blocking effects of mivacurium during sevoflurane or halothane anaesthesia was studied in 38 paediatric patients aged 1–12 yr. All received premedication with midazolam, 0.5 mg · kg⁻¹ po and an inhalational induction with up to 3 MAC of either agent in 70% N₂O and O₂. The ulnar nerve was stimulated at the wrist by a train-of-four stimulus every ten seconds and the force of adduction of the thumb recorded with a Myotrace force transducer. Anaesthesia was maintained with a one MAC end-tidal equivalent of either volatile agent for five minutes before patients received mivacurium (0.2 mg · kg⁻¹) iv. The onset of maximal blockade occurred in 2.4 ± 1.26 (mean ± SD) min with halothane and 1.8 ± 0.54 min with sevoflurane (NS). Four patients failed to achieve 100% block (3 halothane, 1 sevoflurane). The times from injection to 5, 75, and 95% recovery during sevoflurane (9.8 ± 2.6, 19.5 ± 4.4, and 24.2 ± 4.8 min) were greater than during halothane anaesthesia (7.2 ± 2.2, 15.0 ± 4.0, 19.2 ± 4.9 min, respectively (P < 0.005). All patients demonstrated complete spontaneous recovery of neuromuscular function (T₁ > 95%, T₄/T₁ > 75%) during the surgery which lasted 24–63 min. All patients showed clinical signs of full recovery of neuromuscular blockade (i.e., headlift, gag, or cough). Pharmacological reversal was not required. It is concluded that following a single intubating dose of mivacurium, the time to maximum relaxation was not different during halothane and sevoflurane anaesthesia; recovery times to 5, 75 and 95% twitch height were longer during sevoflurane anaesthesia and neuromuscular reversal was not necessary. L’activité neurobloquante du mivacurium pendant l’anesthésie au sévoflurane ou à l’halothane fait l’objet de cette étude réalisée chez 38 enfants de 1 à 12 ans. Tous ont été prémédiqués au midazolam 0,5 mg · kg⁻¹ et l’anesthésie est induite avec un agent volatil jusqu’à MAC 3 de l’un des agents dans du N₂O à 70%. Le nerf cubital était stimulé au poignet au train de quatre aux dix seconds et la force de l’adduction du pouce mesurée avec un transducteur de force Myotrace. L’anesthésie était entretenue avec l’équivalent MAC I d’un des deux agents volatils pendant cinq minutes avant l’administration de mivacurium (0,2 mg · kg⁻¹). Le début du bloc maximum est survenu dans 2,4 ± 1,26 (moyenne ± SD) min avec l’halothane et 1,8 ± 0,54 min avec le sévoflurane (NS). Quatre patients n’ont pas été bloqués à 100% (trois avec l’halothane, un avec le sévoflurane). L’intervalle séparant l’injection à 5; 75, et 95% de la récupération pendant l’anesthésie au sévoflurane (9,8 ± 2,6, 19,5 ± 4,4 et 24,2 ± 4,8 min) a été plus long que pendant l’anesthésie à l’halothane (7,2 ± 2,2, 15,0 ± 4,0, 19,2 ± 4,9 min, respectivement (P < 0,005). An moniteur, chez tous les patients, la fonction neuromusculaire a récupéré spontanément (T₁ > 95%, T₄/T₁ > 75%) au cours de la chirurgie qui a duré de 24–63 min. Tous les patients montraient aussi les signes cliniques d’une récupération complète (par ex., levée de la tête, réflexe pharyngé ou toux). Aucun antagoniste pharmacologique n’a été requis. Il est conclu que le délai jusqu’à la relaxation maximum après une seule dose d’intubation de mivacurium ne diffère pas entre l’anesthésie à l’halothane et l’anesthésie au sévoflurane; les délais de retour à 5, 75 et 95% de la hauteur du twitch sont plus longs pendant l’anesthésie au sévoflurane et il n’est pas nécessaire d’antagoniser le bloc neuromusculaire.

---

Supported in part by a grant from Abbott Laboratories, Chicago, Illinois.     

Atracurium infusion requirements in children during halothane, isoflurane, and narcotic anesthesia

We were interested in determining the dose-response relationship of atracurium in children (2-10 yr) during nitrous oxide-isoflurane anesthesia (1%) and the atracurium infusion rate required to maintain about 95% neuromuscular blockade during nitrous oxide-halothane (0.8%), nitrous oxide-isoflurane (1%), or nitrous oxide-narcotic anesthesia. Neuromuscular blockade was monitored by recording the electromyographic activity of the adductor pollicis muscle resulting from supramaximal stimulation at the ulnar nerve at 2 Hz for 2 sec at 10-sec intervals. To estimate dose-response relationships, three groups of five children received 80, 100, 150 micrograms/kg atracurium, respectively. During isoflurane anesthesia, the neuromuscular block produced by 80 micrograms/kg was 23.6% +/- 6.5 (mean +/- SEM), by 100 micrograms/kg was 45% +/- 7.2, and by 150 micrograms/kg was 64% +/- 8.7. The ED50 and ED95 (estimated from linear regression plots of log dose vs probit of effect) were 120 micrograms/kg and 280 micrograms/kg, respectively. At equipotent concentrations, halothane and isoflurane augment atracurium neuromuscular block to the same extent, compared to narcotic anesthesia. Atracurium steady-state infusion requirements averaged 6.3 +/- 0.6 micrograms . kg-1 . min-1 during halothane or isoflurane anesthesia; the requirements during balanced anesthesia were 9.3 +/- 0.8 micrograms . kg-1 . min-1 (P less than 0.05). There was no evidence of cumulation during prolonged atracurium infusion.     

Effects of halothane, enflurane, and isoflurane on somatosensory evoked potentials during nitrous oxide anesthesia

The effects of 0.5, 0.75, and 1 MAC of halothane, enflurane, and isoflurane in 60% nitrous oxide on somatosensory cortical evoked potentials were studied in 30 patients undergoing corrective surgery for scoliosis. The evoked potentials were averaged at the scalp from the electroencephalogram following repeated bilateral posterior tibial nerve stimulation at the ankle. Latencies and amplitudes of the resulting potentials were measured and compared with the post-induction control values. Graded increase in latencies and graded decrease in amplitudes were found with increasing concentrations of all the three agents (P less than 0.05), confirming that the effects were dose related. Reductions in amplitudes were more marked than increase in latencies. The authors conclude that, during nitrous oxide-based anesthesia, enflurane, and isoflurane resulted in less alteration of somatosensory cortical evoked potentials than halothane. In conjunction with 60% nitrous oxide, 0.5 and 0.75 MAC of halothane, 0.5, 0.75, and 1.0 MAC of isoflurane and enflurane, respectively, were found to be compatible with the generation of waves adequate for evaluation.     

Plasma lidocaine concentrations during epidural blockade with isoflurane or halothane anesthesia.

Because isoflurane maintains hepatic blood flow at higher flows than halothane, we proposed that the elimination of lidocaine would be different between these two volatile anesthetics. The plasma lidocaine concentrations were determined in 14 female patients undergoing epidural blockade plus isoflurane anesthesia and compared with those obtained during halothane anesthesia for lower abdominal surgery. General anesthesia was maintained with isoflurane (0.46% +/- 0.04% [mean +/- SE] inspired, n = 7) or halothane (0.48% +/- 0.05% inspired, n = 7) and 67% nitrous oxide in oxygen. All patients received 2% lidocaine solution, 10 mL as a bolus dose and continuous administration at a rate of 10 mL/h, through the epidural catheter. The plasma lidocaine concentrations over 180 min after the epidural injection in patients receiving isoflurane were similar to those in patients receiving halothane. The results suggest that low inspired concentrations of isoflurane do not reduce plasma lidocaine concentrations in patients during epidural blockade, compared with halothane.     

Plasma cortisol in experimental anesthesia with halothane, enflurane, isoflurane and nitrous oxide

The influence of anesthesia on plasma cortisol has most often been studied in connection with routine operations. To investigate the specific effects of modern inhalation anesthetics more accurately, we examined the specific effects of four inhalation anesthetics on human plasma cortisol during volunteer studies on the influence of anesthetics on the electroencephalogramm. METHODS. A group of 17 (10 m, 7 f) young healthy volunteers who had not received any premedication and were not intubated were studied after informed consent had been obtained. In the first series of experiments the concentration of halothane, enflurane, isoflurane or N2O was increased to MAC (minimal alveolar concentration) 0.5 for a 15-min steady-state period. Blood samples were taken 5 min prior to induction (I), 35 min after induction, on steady-state MAC 0.5 (II), and 15 (III) and 35 (IV) min after the end of anesthesia. In a second series, with 5 subjects, the concentration of halothane, enflurane or isoflurane was first increased to a steady state of MAC 1.0. After reduction to MAC 0.5 steady-state, anesthesia was supplemented with 53% N2O to give a steady state of MAC 1.0 again. Blood samples were taken 5 min prior to induction (I), after the attainment of steady-state MAC 1.0 (II), 35 min later at MAC 0.5 (III), 40 min later at MAC 1.0 with volatile anesthetic/N2O (IV), and 15 (V) and 35 (VI) min after the end of anesthesia. RESULTS. MAC 0.5 N2O produced a marked rise in mean plasma cortisol, from 64.2 micrograms/l to 164.5 micrograms/l.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pharmacokinetic-pharmacodynamic relationship of rocuronium under stable nitrous oxide-fentanyl or nitrous oxide-sevoflurane anesthesia in children

BACKGROUND: The aim of this study was to compare pharmacokinetics and pharmacokinetic-pharmacodynamic (PK-PD) relationship of rocuronium in children anesthetized with nitrous oxide (N2O) and fentanyl or with N2O and sevoflurane. METHODS: Twenty-four children (3-11 years old, ASA PS I or II) were randomized to receive N2O/O2-fentanyl or N2O/O2-sevoflurane (one MAC) anesthesia. Neuromuscular transmission was monitored electromyographically. Initial bolus dose of rocuronium, 0.6 mg x kg(-1) was followed by continuous infusion, targeting at steady-state 95% T1 depression. Neuromuscular transmission was allowed to recover spontaneously. Plasma samples were collected at the moment of discontinuation of infusion, and 10, 20, 30, 50, 60 and 75 min afterwards. Concentrations of rocuronium were measured using high-performance liquid chromatography with electrochemical detection (HPLC-EC). Rocuronium PK was described by a two-compartment model and PD parameters were estimated using effect compartment and sigmoidal E(max) models. RESULTS: No differences in rocuronium PK parameters were observed between study groups. Clearance was 3.91 +/- 2.07 and 3.62 +/- 0.80 ml x min(-1) x kg(-1) in sevoflurane and fentanyl groups, respectively (P < 0.65). Effect compartment concentrations corresponding to 50% inhibition of T1 (EC50) were 1.41 +/- 0.45 and 2.32 +/- 1.00 microg x ml(-1) (P < 0.02), and rate constants for equilibration between plasma and effect compartment (k(e0)) values were 0.10 +/- 0.04 and 0.24 +/- 0.14 min(-1) (P < 0.009) in sevoflurane and fentanyl groups, respectively. CONCLUSIONS: Disposition of rocuronium was similar under stable N2O-fentanyl and N2O-sevoflurane anesthesia. Sevoflurane reduced rocuronium requirements as well as decreased EC50 relevant to inhibition of T1 and rocuronium transfer to effect compartment. Therefore, the potentiating effect of sevoflurane seems to be mainly of PD origin, probably due to an increased sensitivity of the neuromuscular junction.     

Duration of halothane anesthesia and neuromuscular blockade with d-tubocurarine.

Cumulative d-tubocurarine dose-response curves were determined in 35 unpremedicated adult surgical patients. In five awake patients with and five awake patients without ulnar nerve block the median effective doses of d-tubocurarine necessary for 50 per cent depression of twitch tension (ED50) were 8.3 and 9.1 mg/m2, respectively. The presence of an ulnar nerve block did not significantly alter ED50, which suggests that the central nervous system has little influence on the d-tubocurarine dose-response curve. The ED50's of d-tubocurarine were 4.8, 4.5, 2.5, 3.2, and 3.8 mg/m2 in patients anesthetized with 1.0 to 1.3 per cent alveolar concentrations of halothane for 10, 20, 40, 80, and 160 minutes, respectively. It is concluded that duration of anesthesia has no effect on neuromuscular blockade by d-tubocurarine.     

The dose-response relationship of mivacurium chloride in humans during nitrous oxide-fentanyl or nitrous oxide-enflurane anesthesia

The dose-response relationships of mivacurium chloride during N2O/fentanyl or N2O/enflurane anesthesia were compared in 70 patients intraoperatively. Responses were defined in terms of percentage changes in the evoked twitch tension of the adductor pollicis muscle, and dose-response curves were constructed following probit transformation of the responses. End-tidal concentrations of enflurane during the were study were 0.9-1.2%. When compared with the dose-response curve determined during N2O/fentanyl anesthesia the curve determined during N2O/enflurane anesthesia was displaced significantly to the left (P less than 0.05). As a result, the doses of mivacurium that depressed twitch tension by 50% (ED50) and 95% (ED95) were 39 and 67 micrograms/kg, respectively, during N2O/fentanyl anesthesia, and 27 and 52 micrograms/kg during N2O/enflurane anesthesia. Regression lines describing the relationship between the maximum depression of twitch tension (response) and the time interval between the injection of mivacurium and the return of twitch tension to 90% of the control value (duration) were constructed. The response-duration line for N2O/enflurane anesthesia was displaced significantly to the left of the line for N2O/fentanyl (P less than 0.05), indicating that enflurane anesthesia was associated with a prolongation of mivacurium-induced neuromuscular blockade. The neuromuscular blocking effect of mivacurium is both enhanced by and prolonged during N2O/enflurane compared with that during N2O/fentanyl anesthesia.     

Dose-response relationships of doxacurium chloride in humans during anesthesia with nitrous oxide and fentanyl, enflurane, isoflurane, or halothane

In a two-part study, the dose-response relationships of doxacurium chloride (BW A938U) were evaluated during general anesthesia maintained with commonly used anesthetic techniques. In part 1, cumulative dose-response methodology was used to establish the ED95 of doxacurium in 36 patients receiving 70% nitrous oxide and fentanyl, or 50% nitrous oxide and either 1.26% enflurane, 0.84% isoflurane, or 0.57% halothane anesthesia. Mechanomyographic response to train-of-four stimulation was used to monitor neuromuscular blockade. The peak effect of doxacurium following each 5 micrograms/kg incremental dose was noted and a log-probit dose-response curve was constructed for each individual patient. The median ED50s were 11 micrograms/kg, 6 micrograms/kg, 8 micrograms/kg, and 8 micrograms/kg for patients receiving fentanyl, enflurane, isoflurane, or halothane anesthesia, respectively. The median ED95s were 24 micrograms/kg, 14 micrograms/kg, 16 micrograms/kg, and 19 micrograms/kg for patients receiving fentanyl, enflurane, isoflurane, and halothane anesthesia, respectively. In part 2, 72 additional patients received a rapid single injection of the ED95 (n = 36) or 2 X ED95 (n = 36) of doxacurium appropriate for the administered anesthetic as estimated from part one of the study. Peak effects of the ED95 given as single injections correlated well with the results in part 1.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mivacurium infusion requirement and spontaneous recovery of neuromuscular transmission in children anaesthetized with nitrous oxide and fentanyl,halothane, isoflurane or sevoflurane

BACKGROUND: Forty children, aged 3-11 years, ASA I or II, were allocated at random to receive N2O/O2-fentanyl or 1 MAC halothane, isoflurane or sevoflurane-N2O/O2 anaesthesia. Mivacurium was used for muscle relaxation. METHODS: Electromyographic response of the adductor pollicis to train-of-four (TOF) stimulation, 2 Hz for 2 s, applied to the ulnar nerve at 10-s intervals was recorded using the Relaxograph (Datex, Helsinki, Finland). An intubating dose of mivacurium, 0.2 mg.kg-1 was given, and when T1 returned to 5%, muscle relaxation was maintained by continuous infusion of mivacurium, adjusted manually to maintain a stable 90-99% block. RESULTS: Halothane, isoflurane and sevoflurane groups had lower infusion requirements for mivacurium than the N2O-fentanyl group (P=0.000083). Mivacurium requirement was 18.8 +/- 6.8, 10.8 +/- 4.2, 6.9 +/- 3.9 and 9.6 +/- 5.6 microg.kg-1.min-1 for children receiving N2O/O2-fentanyl, halothane, isoflurane and sevoflurane anaesthesia, respectively. CONCLUSIONS: Spontaneous recovery from T1=10% to TOF ratio=0.7 was insignificantly prolonged from 6.3 to 12.5 min in the fentanyl group to 7-16.5 min in children anaesthetized with inhalational anaesthetics.     

异氟醚吸入麻醉与异丙酚静脉麻醉下长时间持续输注罗库溴铵的肌松作用

目的比较异氟醚吸入麻醉与异丙酚静脉麻醉下长时间持续输注罗库溴铵的肌松作用。方法拟在全麻下行口腔-颌面肿瘤择期手术(手术时间达5 h左右)病人30例,ASAⅠ或Ⅱ级,年龄18～65岁,随机分为2组(n=15):异丙酚组(Ⅰ组)异氟醚组(Ⅱ组)。用TOF-Watch SX肌松监测仪进行拇内收肌肌松监测。静脉注射罗库溴铵初始剂量0．6 mg·kg-1后气管插管,持续输注罗库溴铵。调整罗库溴铵的输注速率,T1稳定在基础值的10％时(初始状态),Ⅰ组靶控输注异丙酚维持麻醉,Ⅱ组吸入1 MAC异氟醚维持麻醉,持续5 h,术中维持T1在基础值的10％。记录罗库溴铵输注速率、恢复指数(T1恢复25％至75％的时间,T25-75)以及罗库溴铵停止输注到TOFR为0．9的时间。结果与初始状态比较,Ⅰ、Ⅱ组持续给药30 min-5 h时罗库溴铵输注速率下降(P<0．05);Ⅱ组持续给药1～5 h时罗库溴铵输注速率低于Ⅰ组(P<0．05)。两组间恢复指数和罗库溴铵停止输注到TOFR为0．9的时间差异无统计学意义(P>0．05)。结论罗库溴铵可用于长时间持续输注以维持稳定的肌松。维持T1在基础值的10％的情况下,持续输注罗库溴铵5 h时异氟醚麻醉比异丙酚为主的全凭静脉麻醉罗库溴铵输注速率减少30％,但其恢复指数无差异。     

Nitrous oxide: cardiovascular effects in infants and small children during halothane and isoflurane anesthesia

Two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular function in 31 unmedicated infants and small children. In 15 patients, the cardiovascular effects of equipotent levels of halothane were compared with and without N2O. In 16 patients, the cardiovascular effects of isoflurane with and without N2O were compared. Prior to anesthesia induction, cardiovascular measurements of heart rate (HR), mean blood pressure (MBP), and two-dimensional and pulsed Doppler echocardiography were recorded. The echocardiographic measurements were used to determine cardiac output (CO), stroke volume (SV), ejection fraction (EF), and left ventricular end-diastolic and end-systolic volume (LVEDV and LVESV). Twenty minutes after mask inhalation induction with halothane or isoflurane with N2O and O2 (3:2 liters/min), cardiovascular measurements were repeated with end-expired halothane or isoflurane maintained at 0.9 MAC. A third set of cardiovascular data was collected 10 minutes after the discontinuation of N2O, with inspired isoflurane or halothane levels in O2 (5 liters/min) increased to maintain 1.5 MAC end-expired levels. Ventilation was controlled throughout the study period and the study was completed before intubation and the start of elective surgery. Heart rate and MBP decreased to similar degrees below awake levels in both patient groups during N2O with halothane or isoflurane. When N2O was discontinued and end-expired levels of halothane or isoflurane increased, MBP remained at levels observed during N2O-O2 with halothane or isoflurane. Heart rate increased during isoflurane in O2. Cardiac output decreased significantly and similarly below awake levels during both halothane of isoflurane with and without N2O.     

Electroencephalograms in children during isoflurane anesthesia

The electroencephalograms (EEG) of 55 children under isoflurane anesthesia were studied to elucidate any change in pattern with age. The children ranged from 1 month to 14 years of age were divided into six age groups. The standard minimum alveolar concentration (MAC) was determined in each group. Anesthesia was induced using the slow induction method, and EEG was recorded at isoflurane concentrations of 1.5 MAC in 100% oxygen, 1.0 MAC in 100% oxygen, and 1.0 MAC under administration of 66% nitrous oxide in oxygen. Ventilation was controlled mechanically (end-tidal CO₂ 35–40 mmHg). At 1.5 MAC, the incidences of burst suppression in the groups of 6 months to 6 years of age were significantly less than in groups older or younger than that age (P<0.05). Except for infants less than 6 months of age, the mean values of maximum amplitude at 1.0 MAC were two to three times of those in adults. Children 3–6 years of age showed the highest value of 427.0±83.5 μV. This paper was presented in part at the annual meeting of the Japan Society of Anesthesiology, Osaka, March, 1991.     

The hemodynamic and cardiovascular effects of isoflurane and halothane anesthesia in children

The hemodynamic and cardiovascular effects of isoflurane and halothane anesthesia were studied in 15 unpremedicated ASA I children using measurements of heart rate, blood pressure and M-mode echocardiography (echo). The children (ages 2 to 7.3 yr) were randomly assigned to receive either isoflurane (N = 8) or halothane (N = 7) with oxygen. End-tidal carbon dioxide concentrations (range 30-44 mmHg) were monitored throughout the study in each child. The experimental protocol was completed prior to intubation and the initiation of surgery. Within each anesthetic group, preinduction (control) hemodynamic and echo measurements were compared with measurements obtained at two sequential equipotent end-tidal anesthetic concentrations (0.74% and 2.22% isoflurane; or 0.5% and 1.5% halothane). We also compared the data of the isoflurane group with that of the halothane group at each equipotent end-tidal anesthetic concentration. Preinduction hemodynamic (heart rate, blood pressure) and echo measurements (left ventricular dimensions and function) were similar between the two anesthetic groups. With isoflurane or halothane administration, blood pressure decreased significantly, while heart rate remained essentially unchanged. The observed alterations in heart rate and blood pressure were similar in both study groups at each equipotent end-tidal anesthetic concentration. In contrast, there were marked differences in the echo measurements of the two anesthetic groups. Halothane was associated with a significant dose-dependent decrease in echo-measured left-ventricular shortening fraction and mean velocity of circumferential fiber shortening. These echo measurements were not significantly altered by isoflurane at either end-tidal anesthetic concentration. These alterations suggest halothane is associated with significant myocardial depression in normal children, while myocardial function is well preserved during isoflurane anesthesia.