Effect of bolus dose of remifentanil on haemodynamic response to tracheal intubation

A randomized placebo-controlled double-blinded study was conducted in 40 ASA 1 and 2 patients to determine the dose response of remifentanil in attenuating the haemodynamic response to tracheal intubation. Patients were allocated to one of four groups: placebo, remifentanil 1 microgram.kg-1, remifentanil 2 micrograms.kg-1 and remifentanil 4 micrograms.kg-1. A propofol target-controlled infusion was started at 4 micrograms.ml-1 and incrementally titrated to loss of verbal contact. Muscle relaxation was provided by cisatracurium. The study drug was given three minutes later over 30 seconds, and 90 seconds later the patient's trachea was intubated under direct laryngoscopy. Baseline noninvasive blood pressure and heart rate recordings were made prior to starting target-controlled infusion, then at one-minute intervals after loss of verbal contact for the duration of the study. Demographic data and target-controlled infusion rate at intubation was similar for the groups. Following intubation, heart rate increased by 15% in the placebo group, 10% in 1 microgram.kg-1 group, with no changes in 2 micrograms.kg-1 and 4 micrograms.kg-1 groups. Systolic blood pressure following intubation increased by 30% in the placebo group, 10% in the 1 microgram.kg-1 group and remained unchanged in the 2 micrograms.kg-1 and 4 micrograms.kg-1 groups. Remifentanil 1 microgram.kg-1 attenuated the rise in heart rate and systolic blood pressure. Remifentanil 2 micrograms.kg-1 blocked the haemodynamic response completely: no further benefit was shown from increasing the dose to 4 micrograms.kg-1.     

Evaluation of remifentanil for control of haemodynamic response to tracheal intubation

We have studied the effect of three bolus doses of remifentanil on the haemodynamic response to laryngoscopy and tracheal intubation. Using a double-blind design, 80 ASA 1 or 2 patients presenting for elective surgery received saline placebo or remifentanil 0.25, 0.5 or 1.0 microgram.kg-1 by random allocation. Anaesthesia was induced with thiopentone 5-7 mg.kg-1 and followed immediately by the study medication given as a bolus over 30s. Muscle relaxation was provided with rocuronium 0.75 mg.kg-1. The patients' tracheas were intubated under direct laryngoscopy 1 min later. Noninvasive arterial blood pressure and heart rate were recorded immediately before induction of anaesthesia and then at intervals until 5 min after tracheal intubation. There was a significant increase in heart rate (p < 0.01) and systolic arterial pressure (p < 0.01) in all groups after tracheal intubation. However, this was short-lived and of a smaller magnitude in the remifentanil 1 microgram.kg-1 group in which the increase was significantly lower than in the control group (p < 0.01).     

The effect of remifentanil on the middle latency auditory evoked response and haemodynamic measurements with and without the stimulus of orotracheal intubation

BACKGROUND AND OBJECTIVE: Changes in the middle latency auditory evoked response following the administration of opioids have been shown. However, it remains unclear as to whether these changes are due to a direct depressant effect of opioids on the middle latency auditory evoked response itself, or an indirect effect on account of their action in attenuating central nervous system arousal associated with noxious stimuli. By comparing changes in the middle latency auditory evoked response in intubated and non-intubated patients, receiving saline or remifentanil in different doses, this study attempts to answer this question. METHODS: Fifty-four patients were anaesthetized with isoflurane and nitrous oxide (0.9 MAC) and randomized to 1-6 groups. Groups 1-3 received a bolus injection of either saline 0.9%, low-dose remifentanil (1 microg kg(-1)) or high-dose remifentanil (3 microg kg(-1)) prior to intubation of the trachea. Groups 4-6 were not intubated following the bolus injection. RESULTS: Pa and Nb amplitudes of the middle latency auditory evoked response increased by 82% and 79% with intubation in the saline group (P < 0.005) and these changes were not seen in the patients given remifentanil. There was a significant linear trend for the reduction in Pa and Nb amplitude with increasing remifentanil dose (P < 0.05). In the absence of endotracheal intubation remifentanil had no effect on either the amplitudes or latencies of the waves Pa and Nb and there was no effect of dose. For the haemodynamic measurements remifentanil attenuated the pressor response to intubation (P < 0.001) and had a significant dose-related effect (P < 0.001) in the absence of intubation. CONCLUSIONS: We demonstrated an effect of remifentanil on both the middle latency auditory evoked response and haemodynamic changes to endotracheal intubation. For the non-intubated patients there was only an effect of remifentanil on the haemodynamic measurements. This suggests that remifentanil has an effect on the middle latency auditory evoked response in attenuating the arousal associated with intubation of the trachea but has no effect in the absence of a stimulus.     

Effect of remifentanil on the auditory evoked response and haemodynamic changes after intubation and surgical incision

We have observed the effect of intubation and incision, as measured by the auditory evoked response (AER) and haemodynamic variables, in 12 patients undergoing hernia repair or varicose vein surgery who received remifentanil as part of either an inhaled anaesthetic technique using isoflurane or as part of a total i.v. technique using propofol. Anaesthesia was induced with remifentanil 1 microgram kg-1 and propofol, neuromuscular block was achieved with atracurium 0.6 mg kg-1 before intubation, and anaesthesia was maintained with a continuous infusion of remifentanil in combination with either a continuous infusion of propofol or inhaled isoflurane. The AER and haemodynamic variables were measured before and after intubation and incision. The effects of intubation and incision on the AER and haemodynamic variables were not significantly different between the remifentanil- propofol and remifentanil-isoflurane groups. However, the study had a low power for this comparison. When the data for the two anaesthetic combinations were pooled, the only significant effects were increases in diastolic arterial pressure and heart rate immediately after intubation; these were not seen 5 min after intubation. There were no cardiovascular responses to incision. There were no significant changes in the AER after intubation or incision.      

瑞芬太尼抑制患者清醒气管插管反应的半数有效剂量

目的 确定咪达唑仑镇静下瑞芬太尼抑制患者清醒气管插管反应的半数有效剂量(ED50).方法 择期全麻下行整形外科手术的成年女性患者36例,ASAⅠ级,采用改良Dixon序贯法进行试验,静脉输注咪达唑仑0.1 mg/ks 10 min后,第1例快速静脉输注瑞芬太尼1 μg/kg后以0.1μg·min-1·kg-1静脉输注,若未发生气管插管反应,则下一例瑞芬太尼降低0.1μg/kg,速率降低0.01μg·min-1·kg-1,直至第n例发生气管插管反应.将第n例和第n=1例剂量的平均值作为初始剂量,以0.05μg/kg和0.005μg·min-1·kg-1为梯度进行调整.根据对直接喉镜显露声门及气管插管操作的反应及镇静评分评价是否发生气管插管反应.采用改良Dixon序贯法计算瑞芬太尼抑制清醒气管插管反应的ED50,并采用logistic回归模型进行概率单位转换分析ED50及其95%可信区问.结果 采用改良Dixon序贯法计算瑞芬太尼抑制清醒气管插管反应的ED50为0.62 μg/ks,概率单位转换法计算的ED50及其95%可信区间分别为0.63(0.54～0.70)μg/kg.未发生气管插管反应的19例患者中,有18例对气管插管耐受良好,并可对言语指令作出正确反应.术后随访患者对气管插管操作均无不良记忆.结论 咪达唑仑0.1 mg/kg镇静下,快速静脉输注瑞芬太尼0.62 μg/kg后以0.062 μg·min-1·kg-1静脉输注可为50%的患者提供较好的清醒气管插管条件,且无气管插管反应发生.     

Comparison of haemodynamic responses to orotracheal intubation with GlideScope videolaryngoscope and fibreoptic bronchoscope

BACKGROUND AND OBJECTIVE: The GlideScope videolaryngoscope is a newly developed laryngoscope for tracheal intubation recently introduced into clinical anaesthesia. In this randomised clinical study, we compared the haemodynamic responses to orotracheal intubation using a GlideScope videolaryngoscope and a fibreoptic bronchoscope. METHODS: Fifty-six adult patients, ASA I-II scheduled for elective plastic surgery under general anaesthesia requiring orotracheal intubation were randomly allocated to either the GlideScope videolaryngoscope group or the fibreoptic bronchoscope group. After a standard intravenous anaesthetic induction, orotracheal intubation was performed. Noninvasive blood pressure and heart rate were recorded before and after induction, at intubation and for 5 min after intubation at 1 min intervals. RESULTS: As compared with the post-induction values the orotracheal intubations using a fibreoptic bronchoscope and a GlideScope videolaryngoscope resulted in the significant increases in blood pressures which did not exceed their baseline values. In the two groups, heart rates at intubation and within 2 min after intubation were significantly higher than their baseline values. However, there were no significant differences in blood pressures and heart rates at all time points, their maximal values and maximal percent changes during the observation and the times required to reach their maximal values between the two groups. CONCLUSIONS: The orotracheal intubations using a fibreoptic bronchoscope and a GlideScope videolaryngoscope produce similar haemodynamic responses.     

Effect of fentanyl on the circulatory responses to orotracheal fibreoptic intubation

The effectiveness of fentanyl in attenuating the pressor and heart rate response to orotracheal fibreoptic intubation under general anaesthesia was assessed in 60 healthy patients undergoing elective surgery. Patients were randomly assigned to receive either fibreoptic intubation with or without fentanyl 6 micrograms.kg-1 or traditional Macintosh intubation with fentanyl 6 micrograms.kg-1. A standardised general anaesthetic was administered which included temazepam premedication, thiopentone, atracurium, oxygen, nitrous oxide and isoflurane. The pressor response to fibreoptic intubation was suppressed in those patients who received fentanyl and was similar to that seen in the Macintosh-fentanyl group of patients. The heart rate response to fibreoptic intubation was also significantly reduced in the patients who received fentanyl, but, in contrast, was still significantly greater than that in the Macintosh-fentanyl group. Fentanyl 6 micrograms.kg-1 appears to have a useful place in attenuating the cardiovascular effects of fibreoptic intubation under general anaesthesia.     

Bolus dose remifentanil for control of haemodynamic response to tracheal intubation during rapid sequence induction of anaesthesia

The effect of three bolus doses of remifentanil on the pressor response to laryngoscopy and tracheal intubation during rapid sequence induction of anaesthesia was assessed in a randomized, double-blind, placebo- controlled study in four groups of 20 patients each. After preoxygenation, anaesthesia was induced with thiopental 5-7 mg kg-1 followed immediately by saline (placebo) or remifentanil 0.5, 1.0 or 1.25 micrograms kg-1 given as a bolus over 30 s. Cricoid pressure was applied just after loss of consciousness. Succinylcholine 1 mg kg-1 was given for neuromuscular block. Laryngoscopy and tracheal intubation were performed 1 min later. Arterial pressure and heart rate were recorded at intervals until 5 min after intubation. Remifentanil 0.5 microgram kg-1 was ineffective in controlling the increase in heart rate and arterial pressure after intubation but the 1.0 and 1.25 micrograms kg-1 doses were effective in controlling the response. The use of the 1.25 micrograms kg-1 dose was however, associated with a decrease in systolic arterial pressure to less than 90 mm Hg in seven of 20 patients.      

The effect of remifentanil on the bispectral index change and hemodynamic responses after orotracheal intubation

In order to examine whether changes in the bispectral index (BIS) may be an adequate monitor for the analgesic component of anesthesia, we evaluated the effect of remifentanil on the BIS change and hemodynamic responses to laryngoscopy and tracheal intubation. Fifty ASA physical status I patients were randomly assigned, in a double-blinded fashion, to one of five groups (n = 10/group) according to the remifentanil target effect compartment site concentration (0, 2, 4, 8, or 16 ng/mL). The target-controlled infusion (TCI) of remifentanil was initiated 3 min after the TCI of propofol that was maintained at the effect-site concentration of 4 microg/mL throughout the study. After the loss of consciousness and before the administration of vecuronium 0.1 mg/kg, a tourniquet was applied to one arm and inflated above the systolic blood pressure in order to detect any gross movement within the first minute after tracheal intubation, which was performed 3 min after remifentanil TCI began. A BIS value was generated every 10 s. Arterial blood pressure and heart rate (HR) were measured every minute, noninvasively. Measures of mean arterial pressure (MAP), HR, and BIS were obtained before the induction, before the start of remifentanil TCI, before laryngoscopy, and 5 min after intubation. The relationships between remifentanil effect-site concentrations and BIS change or hemodynamic responses (changes in MAP and HR) to intubation were determined by logarithmic regression. BIS values were not affected by remifentanil before laryngoscopy. During this period, MAP and HR decreased significantly (P < 0.01) in the remifentanil 8 and 16 ng/mL groups. Changes in BIS, MAP, and HR were negatively correlated with remifentanil effect-site concentration (P < 0.0001). The number of movers in the remifentanil 0-, 2-, 4-, 8-, and 16-ng/mL groups was, respectively, 10, 9, 7, 1, and 0. Hypotensive episodes (MAP < 60 mm Hg) were noted in 1, 2, and 5 patients in the remifentanil 4-, 8-, and 16-ng/mL groups, respectively. We conclude that the addition of remifentanil to propofol affects BIS only when a painful stimulus is applied. Moreover, remifentanil attenuated or abolished increases in BIS and MAP after tracheal intubation in a comparable dose-dependent fashion. IMPLICATIONS: Bispectral index change is as sensitive as hemodynamic responses after a painful stimulus for detecting deficits in the analgesic component of anesthesia. It may, therefore, be a useful monitor of the depth of anesthesia in patients who are incapable of HR and MAP responses to noxious stimuli because of medications or cardiovascular disease.     

Cigarette smoking and the haemodynamic response to tracheal intubation

This study investigated the effects of smoking and gender on the haemodynamic response after tracheal intubation. Patients were assigned to one of four groups: female non-smokers, female smokers, male non-smokers and male smokers. After tracheal intubation, the highest mean (SD) increase in heart rate (30 (18) %) and rate–pressure product (40 (29) %) was seen in male smokers. The increases in heart rate and rate–pressure product in male smokers were significantly greater than those in female non-smokers, p < 0.05. The increase in rate–pressure product was significantly greater in male smokers than in male non-smokers, p = 0.022.     

Esmolol prevents movement and attenuates the BIS response to orotracheal intubation

Background. Beta-adrenergic agonists enhance behavioural andelectroencephalographic arousal reactions. We explored whetheradding esmolol, a short-acting ß₁-adrenoceptor antagonist,to propofol anaesthesia modified the bispectral index (BIS)during induction of anaesthesia and orotracheal intubation. Methods. Fifty patients were randomly allocated, in a double-blindfashion, to receive esmolol 1 mg kg^–1 followed by 250µg kg^–1 min^–1 or saline (control). Esmololor saline was started 6 min after a target-controlled infusion(TCI) of propofol (effect-site concentration 4 µg ml^–1).After loss of consciousness, and before administration of vecuronium0.1 mg kg^–1, a tourniquet was applied to one arm and inflatedto 150 mm Hg greater than systolic pressure. Eleven minutesafter the TCI began, the trachea was intubated; gross movementwithin the first min after orotracheal intubation was recorded.BIS was recorded at 10-s intervals. Mean arterial pressure (MAP)and heart rate were measured non-invasively every min. Results. There were no intergroup differences in BIS, heartrate or MAP before laryngoscopy. BIS increased significantlyafter orotracheal intubation (compared with the pre-laryngoscopyvalues) in the control group only, with a maximum increase of40 (SD 18)% vs 8 (11)% in the esmolol group (P<0.01). Maximumchanges in heart rate [45 (19)% vs 23 (14)%] and MAP [62 (24)%vs 45 (23)%] with orotracheal intubation were also significantlygreater in the control group than in the esmolol group. Morepatients in the control than in the esmolol group moved afterorotracheal intubation (23 vs 12, P<0.01). Conclusion. Esmolol not only attenuated haemodynamic and somaticresponses to laryngoscopy and orotracheal intubation, but alsoprevented BIS arousal reactions in patients anaesthetized withpropofol. Br J Anaesth 2002; 89: 857–62     

雷米芬太尼对老年患者气管插管心血管反应的影响

目的观察不同剂量雷米芬太尼微量泵输注对老年患者气管插管时的心血管反应。方法 60例全麻老年患者随机均分为六组。泵注丙泊酚33 mg/min至意识消失后,Ⅰ、Ⅱ、Ⅲ组分别输注雷米芬太尼0.15、0.20、0.25μg.kg-1.min-1,持续6 min;Ⅳ、Ⅴ、Ⅵ组分别输注雷米芬太尼0.15、0.20、0.25μg.kg-1.min-1,持续8 min。丙泊酚维持量0.12 mg.kg-1.min-1。雷米芬太尼输注结束时静注罗库溴铵0.6 mg/kg,气管插管。记录诱导前(T0)、气管插管前1 min(T1)、气管插管后1 min(T2)、2 min(T3)、3 min(T4)、4 min(T5)、5 min(T6)的SBP、DBP和HR变化。结果与T0时比较,T1时六组SBP、DBP明显下降、HR明显减慢(P0.05或P0.01),T2和T4时Ⅲ、Ⅴ、Ⅵ组HR均明显减慢(P0.05或P0.01)。与T1时比较,T2~T3时Ⅰ、Ⅱ组SBP和DBP、T2~T4时Ⅳ组SBP均明显升高(P0.05或P0.01);Ⅰ、Ⅳ、Ⅴ组T2~T6时、Ⅱ组T2~T3时、Ⅲ组T3~T6时和Ⅵ组T3~T5时的HR明显增快(P0.05或P0.01)。结论老年患者气管插管时,雷米芬太尼复合丙泊酚微量泵输注时,雷米芬太尼以0.20或0.25μg.kg-1.min-1的速度,泵注6 min以上可以有效地抑制气管插管时的心血管反应。     

Second dose thiopentone attenuates the haemodynamic response to laryngoscopy and intubation

The study was undertaken to evaluate the effectiveness of large (divided) thiopentone dosage on the peripheral haemodynamic response to laryngoscopy and intubation. Seventy-six (76) patient aged 18 to 67 years were sequentially assigned to either the second dose thiopentone group (n = 36) or the control group (n = 40). The first group had 4 mg.kg-1 thiopentone for induction of anaesthesia, then 1.5 mg.kg-1 suxamethonium chloride for muscle relaxation and a second dose of thiropentone (4 mg.kg-1) just before laryngoscopy and intubation. The control group had thiopentone 4 mg.kg-1 for induction of anaesthesia, suxamethonium 1.5 mg.kg-1 for muscle relaxation and then laryngoscopy and intubation. The heart rate (HR), systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), and rate pressure product (RPP) were measured before induction of anaesthesia and after laryngoscopy and intubation. The difference in the values represented the haemodynamic response to laryngoscopy and intubation. The second dose thiopentone technique compared with the control group, significantly attenuated the post-intubation rise in HR (19.7 vs. 30.9), SAP (18.0 vs. 37.5) and RPP (4795.4 vs. 8440.0). The post intubation rise in DAP (33.9 vs. 42.5) and MAP (31.9 vs. 42.0) didn't show significant difference between the two groups.     

小剂量瑞芬太尼和芬太尼预防小儿经口气管插管血液动力学反应的比较

目的 比较小剂量瑞芬太尼和芬太尼对小儿经口气管插管血液动力学反应的影响。方法 择期在全身麻醉下行整形外科手术患儿90例，ASAⅠ或Ⅱ级，年龄3-9岁，随机分为3组（n=30）：对照组（C组）、芬太尼组（F组）和瑞芬太尼组（R组）。气管插管前5min行麻醉诱导，C组和F组分别静脉注射生理盐水0．2ml／kg或芬太尼2μg／kg，插管前2min三组均静脉注射维库溴铵0．1mg/kg和异丙酚2．5mg／kg，插管前1．5minR组在30s内静脉输注瑞芬太尼1μg/kg。采用直接喉镜行经口气管插管。记录麻醉诱导前（基础值）、诱导后即刻、气管插管时和插管后1、2、3、4、5min时的血压和心率（HR），计算各对应时点HR和收缩压（SBP）的乘积（RPP）。记录插管时间、从插管操作开始至出现SBP和HR最大值的时间（TMAX-SBP和TMMAX-HR）以及从插管操作完成至SBP和HR恢复至诱导后即刻值的时间（TR-SHP和TRR-HR）。结果 与基础值相比，诱导后即刻各组血压均降低，F组和R组降低较C组明显（P〈0．05），C组HR增快（P〈0．05），F组和R组HR保持稳定；气管插管致各组血压、HR和RPP升高（P〈0．05），以C组最为明显，R组最轻；R组TMNAX-SBP和TMMAX-HR长于C组和F组，THR-SBP和TR-HR短于C组和F组（P〈0．05）。结论 与小剂量芬太尼相比，小剂量瑞芬太尼可更有效地抑制小儿经口气管插管的血液动力学反应。     

Cardiovascular response to orotracheal intubation using midazolam or etomidate in anesthesia induction

By means of the present study, we compare the variations in the cardiovascular response to the orotracheal intubation while using midazolam or etomidate during the anesthetic induction. For this purpose, we studied 2 groups of 10 patients each one which were premedicated with fentanyl and atropine, and succinylcholine as muscle relaxant. We took the data at a basal state, 10 minutes after premedication and 0, 1, 2, 3, 4, 5 and 10 minutes after the intubation handling. As hemodynamic data we registered heart rate, systolic and diastolic blood pressure and the rate product (PRP). In both groups, the peak response occurred two minutes after intubation in all the studied parameters. Systolic and diastolic blood pressure as well as PRP were significantly lower with midazolam. We conclude that midazolam and etomidate do not prevent the cardiovascular response to the intubation handling, although midazolam smooths pressure response.     

不同剂量雷米芬太尼对气管插管反应的影响

目的 观察不同剂量雷米芬太尼用于全麻诱导气管插管时的心血管反应,探讨其最佳的全麻诱导剂量.方法 将96例择期行腹部手术的患者随机均分为四组.全麻诱导均采用咪唑安定0.06 mg/kg、依托咪酯0.3 mg/kg、维库溴铵0.1 mg/kg;雷米芬太尼剂量分别为1μ9/kg(R1组)、2μg/kg(R2组)、3μ9/kg(R4组)和4μg/kg(R4组).记录诱导前(T0)、诱导后气管插管前(T1)、气管插管后即刻(T2)、气管插管后1min(T3)、2min(T4)、3min(T5)、5min(T6)和10min(T7)的SBP、DBP、HR的变化.结果 与T0比较,各组T1时SBP、DBP均明显下降(P<0.05或P<0.01),R1组T2、T3时SBP显著升高(P<0.05).与T0比较,各组患者T1时的HR均明显减慢(P<0.01),R1组患者T2、T3时HR显著增快(P<0.05或P<0.01).R2、R3组气管插管期间血压波动幅度均较R1、R4组小(P<0.05).结论 采用2～3μg/kg的雷米芬太尼麻醉诱导可有效抑制气管插管时的心血管反应.