Effect of remifentanil on the haemodynamic response to orotracheal intubation

We have examined the effect of remifentanil on the haemodynamic response to orotracheal intubation in a randomized, double-blind study. We studied 40 patients allocated to one of four groups of 10 each, to receive the following immediately before induction of anaesthesia: remifentanil 1 microgram kg-1 bolus over 30 s, followed by an infusion of 0.5 microgram kg-1 min-1; saline placebo only; glycopyrrolate 200 micrograms and remifentanil 1 microgram kg-1 bolus over 30 s, followed by an infusion of 0.5 microgram kg-1 min-1; or glycopyrrolate 200 micrograms only. Anaesthesia was induced with propofol, vecuronium and 1% isoflurane with 66% nitrous oxide in oxygen. The trachea was intubated under direct laryngoscopy 3 min after induction of anaesthesia. Arterial pressure and heart rate were measured non- invasively, immediately before induction of anaesthesia and then at 1- min intervals. Remifentanil was found to effectively attenuate the pressor response to intubation (P < 0.05 for the increase in mean arterial pressure; P < 0.01 for the increase in heart rate). In the absence of a concurrent vagolytic agent, remifentanil was associated with bradycardia or hypotension, or both, in five of 10 patients, compared with one patient who received remifentanil and glycopyrrolate.      

A comparison of remifentanil and fentanyl in patients undergoing carotid endarterectomy

BACKGROUND AND AIM: We investigated the haemodynamic stability and emergence characteristics of isoflurane/nitrous oxide anaesthesia supplemented with remifentanil or fentanyl in patients undergoing carotid endarterectomy. METHODS: Anaesthesia was induced with propofol (1-2 mg kg-1) and either remifentanil (0.5 microgram kg-1) or fentanyl (1 microgram kg-1), followed by an infusion of remifentanil (0.2 microgram kg-1 min-1) or fentanyl (2 micrograms kg-1 h-1). RESULTS: There were no significant differences between the groups in haemodynamic variables, postoperative pain, nausea or vomiting. After induction there was a significant decrease in mean arterial pressure for both groups (P < 0.001) and a decrease in heart rate (P = 0.001) in the remifentanil group. In both groups these haemodynamic changes continued during maintenance of anaesthesia (P < 0.05). The time to eye opening after surgery was significantly shorter with remifentanil compared with fentanyl (6.62 +/- 3.89 vs. 18.0 +/- 15.18 min, P = 0.015). CONCLUSION: Remifentanil appears to be a comparable opioid to fentanyl when supplementing isoflurane/nitrous oxide anaesthesia for carotid endarterectomy.     

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.      

Comparison of different doses of remifentanil on the cardiovascular response to laryngoscopy and tracheal intubation

We have compared three bolus and infusion regimens of remifentanil on the cardiovascular response to laryngoscopy and orotracheal intubation in three groups of 20 ASA I-II female patients, in a randomized, double- blind study. Patients in group 1 received glycopyrolate 200 micrograms i.v. followed by a bolus dose of remifentanil 1 microgram kg-1 over 30 s and an infusion of remifentanil at a rate of 0.5 microgram kg-1 min- 1. The other patients received remifentanil 0.5 microgram kg-1 over 30 s and an infusion of 0.25 microgram kg-1 min-1 with (group 2) or without (group 3) pretreatment with glycopyrrolate 200 micrograms. All patients then received a sleep dose of propofol, rocuronium 0.6 mg kg-1 and 1% isoflurane with 67% nitrous oxide in oxygen. Laryngoscopy and tracheal intubation were performed 3 min later. Heart rate and arterial pressure were recorded at 1-min intervals from before induction of anaesthesia until 5 min after intubation. Baseline heart rate was similar in all groups, but decreased in group 3 (no glycopyrrolate) after induction and remained significantly lower after intubation compared with the other groups (P < 0.05). Heart rate and arterial pressure increased slightly after intubation in each group but there were no significant differences in mean arterial pressure between groups at any time. The incidence of bradycardia (one patient in group 2) and hypotension (two patients in groups 1 and 2 and three patients in group 3) was low.      

Clinical comparison of either small doses of fentanyl or remifentanil for blunting cardiovascular changes induced by tracheal intubation

BACKGROUND: To compare in a prospective, randomized study the effects on cardiovascular changes after tracheal intubation produced by small doses of either remifentanil or fentanyl. METHODS: With Ethical Committee approval, after intravenous midazolam premedication (0.05 mg.kg-1), 30 normotensive, ASA physical status I-II patients, without cardiovascular or respiratory diseases, and with a Mallampati score < 2, were randomly allocated to receive an intravenous bolus of either 3 micrograms.kg-1 fentanyl (n = 15) or 1 microgram.kg-1 remifentanil (n = 15) infused over 60 sec and followed by a 0.15 microgram.kg-1.min-1 continuous intravenous infusion. General anesthesia was then induced with propofol (2 mg.kg-1), followed by atracurium besilate (0.5 mg.kg-1) to facilitate tracheal intubation. Following intubation, the lungs were ventilated mechanically using a 60% nitrous oxide in oxygen mixture with a 1% inspired fraction of sevoflurane. Arterial blood pressure and heart rate were recorded before anesthesia induction (baseline), one minute after induction of anesthesia, immediately after tracheal intubation and every minute for the first five minutes after intubation. RESULTS: Systolic arterial blood pressure values were significantly higher in the Fentanyl than in the Remifentanil group patients from 2 to 5 min after tracheal intubation (p < 0.01), while no differences were observed between the two groups in either diastolic arterial blood pressure or heart rate values. Four patients in the Remifentanil group (26%) but only one patient in the Fentanyl group (7%) showed systolic blood pressure values < 90 mmHg during the study period (p = not significant); however, the observed decreases in systolic arterial blood pressure values were transient and did not require treatment for any subject. CONCLUSION: We conclude that in healthy normotensive patients, the control of cardiovascular responses to tracheal intubation obtained with a 1 microgram.kg-1 loading dose of remifentanil is more effective than that provided by a 3 micrograms.kg-1 bolus of fentanyl, with the advantage of no risks for postoperative respiratory depression.     

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 effects of remifentanil on haemodynamic stability during rigid bronchoscopy

We examined the effect of remifentanil on the haemodynamic response to rigid bronchoscopy in 22 adult ASA 2-4 patients, randomly allocated to receive 1.0 microg.kg-1 remifentanil over 1 min followed by 0.5 microg.kg-1.min-1 (remifentanil group) or 2.0 microg.kg-1 fentanyl followed by a saline infusion (control group). Following the initial infusion, all patients received a sleep dose of propofol followed by rocuronium 0.6 mg.kg-1 and their lungs were ventilated using a Sander's injector attached to the rigid bronchoscope. Direct arterial blood pressures, heart rate and ST segment changes on the CM5 lead configuration of the electrocardiograph were measured at 1-min intervals from before induction of anaesthesia until the end of bronchoscopy. Arterial pressures and heart rate were similar in the two groups before and after induction of anaesthesia. Remifentanil attenuated the haemodynamic response to bronchoscopy (p < 0.05 for increases in arterial pressures and heart rate). Four patients in the remifentanil group had ST segment depression compared with eight patients in the control group, but this was not statistically significant.     

Induction of anaesthesia in patients with coronary artery disease: a comparison between sevoflurane-remifentanil and fentanyl-etomidate.

In a prospective, randomized study, sevoflurane-remifentanil (Group SR) was compared with fentanyl-etomidate (Group FE) for induction of anaesthesia in patients with ischaemic heart disease. Cardiovascular stability, heart rate, mean arterial pressure, rate pressure product, rescue medications and associated myocardial ischaemia were measured. For Group SR (n = 20), anaesthesia was induced with vital capacity breaths of sevoflurane 5% in oxygen. After loss of consciousness, the inspired sevoflurane was reduced to 3% and remifentanil was administered as a 0.5 microgram.kg-1 bolus over 90 seconds (0.33 microgram.kg-1.min-1) followed by a 0.025 microgram.kg-1.min-1 infusion. After intubation, the inspired sevoflurane was reduced to 2%. For Group FE (n = 20), anaesthesia was induced with fentanyl 10.5 micrograms.kg-1 and etomidate 0.2 mg.kg-1 given 60 seconds later. Isoflurane 1% in oxygen was administered after loss of consciousness. Both groups received rocuronium and the trachea was intubated two minutes later. Sevoflurane gaseous induction was smooth, with cardiovascular stability comparable to fentanyl-etomidate. Significantly more patients in Group SR (P < 0.05) were on beta-blocking medication, and, overall, the HR and RPP was lower pre-intubation in Group SR. Remifentanil administration was associated with severe bradycardia in three patients and asystole in a fourth. All four patients were on beta-blocking medication and three of the four were on diltiazem. The study was terminated due to the high incidence of bradycardic/asystolic complications in Group SR.     

An open, randomized comparison of alfentanil, remifentanil and alfentanil followed by remifentanil in anaesthesia for craniotomy

We studied 52 adults undergoing elective craniotomy, allocated randomly to one of three opioid treatments: alfentanil 50 micrograms kg-1 followed by 0.833 microgram kg-1 min-1 until dural closure (group Alf.); alfentanil 50 micrograms kg-1 followed by 0.833 microgram kg-1 min-1 for 2 h, then remifentanil 0.25 microgram kg-1 min-1 (group Alf.- Remi.); or remifentanil 1 microgram kg-1 followed by 0.5 microgram kg-1 min-1 reducing to 0.25 microgram kg-1 min-1 after craniotomy (group Remi.). Anaesthesia was maintained with infusion of propofol and 66% nitrous oxide in oxygen. Infusions of propofol and remifentanil were stopped at head bandaging. Group Remi. had the least intraoperative haemodynamic responses and group Alf. the most (P < 0.05). Times to tracheal extubation and obey commands were similar in all groups. In all patients in group Alf.-Remi. and group Remi., the trachea was extubated 27 min from the end of anaesthesia; three patients in group Alf. were slower to recover. Use of analgesia in the recovery room and time to transfer to the neurosurgical unit were similar in the three groups.      

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.      

Use of remifentanil in combination with desflurane or propofol for ambulatory oral surgery

We evaluated the use of remifentanil administered as a component of an inhalation or of a Target Controlled Infusion (TCI) anesthetic technique during outpatient oral surgery. Sixty-three unpremedicated patients undergoing removal of four impacted third molars participated to this prospective, randomized study. Anesthesia was induced with Propofol and Rocuronium. Remifentanil 1 microgram.kg-1 i.v. was given over 30 s followed by a continuous infusion reduced from 25% each time a tooth was removed (0.25-->0.0625 microgram.kg-1 min-1). Anesthesia was maintained with Desflurane (group D, n = 31) (end-tidal concentration 4-6%) or Propofol (group P, n = 32) (initial infusion TCI 8 micrograms.ml-1 reduced to 2-3 micrograms.ml-1 after intubation). Corticosteroids, a non-steroidal anti-inflammatory drug (NSAID) (Diclofenac) and a partial mu agonist drug (Tramadol) were administered i.v. during the procedure to prevent early postoperative pain. Recovery time, postoperative pain, recovery of cognition and nausea or vomiting were also evaluated during the first six postoperative hours. Overall mean systolic blood pressures and heart rate were similar in the two groups during surgery. Mean times to extubation and to recall of birth-date and room number were also similar. The quality of awakening was good in the two groups. Most patients complained of moderate pain or had no pain during the first six postoperative hours. The incidence of nausea and vomiting was similar in both groups. No other side effect was observed. These data suggest that the association of Remifentanil, Methylprednisolone, Diclofenac and Tramadol is an useful technique in ambulatory oral surgery in two comparable anesthetic regimens.     

Randomized placebo-controlled trial to assess the effect of remifentanil and propofol on bispectral index and sedation

The effect of the combination of opiates and hypnotics on bispectral index (BIS) is unclear. This double-blind placebo-controlled trial investigated the effect on BIS and sedation of different infusion doses of remifentanil combined with a steady infusion of propofol. Forty patients initially received a target-controlled infusion of propofol 2 micrograms ml-1 for 15 min. They were then randomized to receive either placebo, 0.01, 0.05 or 0.1 microgram kg-1 min-1 remifentanil for a further 15 min. We found a significant correlation between the dose of remifentanil and the change of BIS after 15 min of infusion. The correlation between all the sedation scores and their corresponding BIS was also significant. We concluded that remifentanil, in combination with propofol, reduces BIS when used for sedation.      

Target-controlled propofol requirements at induction of anaesthesia: effect of remifentanil and midazolam

BACKGROUND AND OBJECTIVE: Target-controlled infusions of anaesthetic agents have become increasingly available. They can involve the use of propofol in combination with an opioid or a benzodiazepine. The effect site concentration of propofol infusions has been advocated as a method of estimating drug distribution. We investigated the influence of co-induction with remifentanil and midazolam on effect site propofol requirements at induction of anaesthesia using target-controlled infusions. METHODS: Sixty-six consenting adult patients were randomly allocated to three treatment groups. Each group received induction of anaesthesia with a different total intravenous technique. One group was induced with target-controlled propofol alone; another received target-controlled propofol and target-controlled remifentanil (3 ng mL-1); and the last received midazolam (0.03 mg kg-1), target-controlled remifentanil (3 ng mL-1) and target-controlled propofol. Computer simulation was used to calculate effect site concentrations. We recorded propofol dose and effect site concentration at loss of verbal response. RESULTS: The effect site concentration (Ce50) of propofol alone was 2.19 micrograms mL-1. This was reduced to 1.55 micrograms mL-1 during co-induction with remifentanil and further reduced to 0.64 microgram mL-1 with midazolam premedication (P < 0.001; ANOVA). CONCLUSIONS: We conclude that co-induction with remifentanil alone or with midazolam can be used to reduce propofol doses at induction of anaesthesia using target-controlled infusions. We believe that using effect site concentration may prove a useful tool in routine clinical practice.     

Remifentanil in combination with propofol for spontaneous ventilation anaesthesia

We have investigated the effect of four doses of remifentanil on the incidence of respiratory depression and somatic response at incision. Remifentanil was administered as a loading dose of 0.125, 0.25, 0.375 or 0.5 microgram kg-1 and at a maintenance infusion rate of 0.025, 0.05, 0.075 or 0.1 microgram kg-1 min-1, respectively, with an infusion of propofol 6 mg kg-1 h-1. Responses occurred in 88% of patients with remifentanil 0.025 microgram kg-1 min-1 compared with 30-40% in the other groups. Respiratory depression after incision increased from 6% with remifentanil 0.025 microgram kg-1 min-1 to 73% with 0.1 microgram kg-1 min-1. Increases in propofol infusion rate to 7.2-8.4 mg kg-1 h-1 produced adequate maintenance of anaesthesia. Reductions in remifentanil doses to 0.025-0.05 microgram kg-1 min-1 resulted in adequate respiration at the end of surgery in 88% of patients. Maintenance infusions of the two drugs for spontaneous ventilation are likely to be in these ranges. However, the ideal loading doses and infusion rates for induction remain to be established.      

Small doses of remifentanil or sufentanil for blunting cardiovascular changes induced by tracheal intubation: a double-blind comparison

BACKGROUND AND OBJECTIVE: To compare the effects on cardiovascular changes induced by tracheal intubation when small doses of either remifentanil or sufentanil are used in the presence of midazolam. METHODS: Thirty normotensive, ASA physical status I-II patients, receiving general anaesthesia for major abdominal surgery, received an intravenous midazolam premedication (0.05 mg kg-1) 10 min before induction. They were randomly allocated to receive in a double-blind fashion an intravenous bolus of either (a) remifentanil given as a bolus dose 1 microgram kg-1 (n = 15), or else (b) sufentanil 0.1 microgram kg-1 infused over 60 s (n = 15). In each instance this loading dose was followed by a continuous intravenous infusion (0.1 microgram kg-1 min-1 or 0.01 microgram kg-1 min-1 of remifentanil or sufentanil, respectively). General anaesthesia was induced with propofol (2 mg kg-1), followed by atracurium besilate (0.5 mg kg-1) to facilitate tracheal intubation. Following intubation, the lungs were mechanically ventilated with a 60% nitrous oxide in oxygen mixture and a 1% inspired sevoflurane. RESULTS: Arterial pressure and heart rate were recorded before induction of anaesthesia (baseline), immediately before intubation, immediately after tracheal intubation and every minute for the first five minutes thereafter. No differences in systolic and diastolic arterial pressures were observed between the two groups. At the end of the study period, systolic and diastolic pressures slightly decreased from preinduction values in both groups. Four patients in the remifentanil group (26%) and five patients in sufentanil group (33%) showed at least one systolic pressure value < 90 mmHg during the study period (P = not significant); however, the observed decreases in systolic pressure were transient and did not require treatment. Heart rate values were not affected by tracheal intubation in either group. CONCLUSIONS: In healthy normotensive patients without cardiovascular disease the use of a relatively small dose of either remifentanil or sufentanil after standard midazolam premedication results in a similar and clinically acceptable effectiveness in blunting the cardiovascular changes induced by tracheal intubation.     

Concentration of remifentanil needed for tracheal intubation with sevoflurane at 1 MAC in adult patients

BACKGROUND AND OBJECTIVE: Inhalation induction with sevoflurane provides acceptable conditions for tracheal intubation. Opioids significantly decrease the alveolar concentration needed to achieve tracheal intubation. The purpose of this study was to determine the target concentration of remifentanil providing excellent conditions for tracheal intubation with sevoflurane at 1 minimum alveolar concentration without muscle relaxant. METHODS: Twenty-four consecutive patients, aged 18-50 yr, ASA I or II, were studied. Induction of anaesthesia was performed with sevoflurane at age-adjusted minimum alveolar concentration. Remifentanil was simultaneously administered using target-controlled infusion with the Minto model. Target plasma concentration of remifentanil was selected for each patient according to an up-and-down method. RESULTS: The mean target concentration of remifentanil for successful tracheal intubation was 3.3 ng mL(-1) (95% confidence interval: 2.6-3.9 ng mL(-1)). Arterial pressure, heart rate and bispectral index did not increase after tracheal intubation in the group of patients with successful intubation. CONCLUSIONS: Remifentanil at 3.3 ng mL(-1) together with sevoflurane at 1 minimum alveolar concentration provides excellent conditions for tracheal intubation in 50% of patients.     

Remifentanil reduces auditory and somatosensory evoked responses during isoflurane anaesthesia in a dose-dependent manner

We studied 60 patients during stable isoflurane anaesthesia (0.4 MAC) after premedication with temazepam. Patients were allocated randomly to one of three dose regimens of remifentanil: 1 microgram kg-1 i.v. over 1 min and an infusion of 0.2 microgram kg-1 min-1 (low dose); 2.5 micrograms kg-1 and 0.5 microgram kg-1 min-1 (medium dose); and 5 micrograms kg-1 and 1 microgram kg-1 min-1 (high dose). The auditory (AER) and median nerve somatosensory (SER) responses were elicited throughout, and recorded before and after tracheal intubation, and surgical incision, together with systolic and diastolic arterial pressure and heart rate. Venous blood concentrations of remifentanil were measured at the above times. After administration of remifentanil, Pa and Nb amplitudes of the AER increased at the low dose, remained constant at the medium dose and decreased at the high dose. This dose- related effect was linear and significant (P = 0.012, P = 0.05). Pa amplitude correlated inversely with remifentanil blood concentrations before and after intubation and incision (P = 0.002, P < 0.001, P < 0.001 and P < 0.001). In the SER, P15-N20 amplitudes decreased after administration of remifentanil (P < 0.001), whereas P25-N35 and N35-P45 amplitudes increased at all dose concentrations (P < 0.001 and P < 0.001). After intubation, P15-N20 and N35-P45 amplitudes increased at the low dose, did not change at the medium dose and decreased at the high dose (P = 0.001, P = 0.027). After remifentanil, systolic and diastolic arterial pressure and heart rate decreased in a linearly dose- related manner (P = 0.033, P < 0.001, P < 0.001). At all doses the three variables increased after intubation (P = 0.001, P < 0.001, P < 0.01), and systolic and diastolic arterial pressure increased after incision (P = 0.027, P = 0.039).      

Effect of a remifentanil bolus dose on the cardiovascular response to emergence from anaesthesia and tracheal extubation

We have examined the effect of remifentanil on the haemodynamic response to emergence from anaesthesia and tracheal extubation in 40 ASA I-II female patients undergoing diagnostic laparoscopy, in a randomized, double-blind study. All patients received a standard general anaesthetic comprising propofol, vecuronium and 1% isoflurane with 66% nitrous oxide in oxygen. At the end of surgery, a bolus dose of remifentanil 1 microgram kg-1 (n = 20) or saline placebo (n = 20) was given and tracheal extubation was performed when standard criteria were achieved. Arterial pressure and heart rate were recorded non- invasively at 1-min intervals from the end of surgery. Remifentanil attenuated the increase in both mean arterial pressure (P < 0.001) and heart rate (P < 0.05) at extubation. Mean time to extubation was 7.2 (SEM 0.6) min and 4.0 (0.5) min in the remifentanil and saline groups, respectively (P < 0.001). There was no difference in the incidence of coughing at extubation, time to recovery from anaesthesia or time to fitness for discharge from the recovery room.      

Comparison of remifentanil with alfentanil or suxamethonium following propofol anaesthesia for tracheal intubation.

Sixty ASA physical status I and II, premedicated patients were administered propofol 2 mg x kg-1 and remifentanil 2 microg x kg-1 (group R), alfentanil 50 microg x kg-1 (group A) or suxamethonium 1 mg x kg-1 (group S) as a rapid bolus. One minute after study drug administration, tracheal intubation was performed. Intubation conditions were then scored. Excellent or good conditions were observed in only 35% in group R compared with groups S and A (100% and 85%, respectively; p < 0.001). The haemodynamic response to tracheal intubation was blunted in groups R and A compared with group S (p < 0.001). The mean heart rate in groups R and A was significantly lower than group S (p < 0.001). We conclude that remifentanil 2 microg x kg-1 given as a rapid bolus will not produce intubating conditions as good as those obtained with alfentanil 50 microg x kg-1 or suxamethonium 1 mg x kg-1 if administered after propofol 2 mg x kg-1.     

Reducing the haemodynamic responses to laryngoscopy and intubation

The effects of alfentanil and fentanyl on controlling the haemodynamic responses to laryngoscopy and intubation have been compared. Five groups of ten patients were studied. Induction was with thiopentone 4 mg/kg. Thirty seconds later group 1 received 1 ml/20 kg saline, group 2 received 15 micrograms/kg alfentanil, group 3 received 30 micrograms/kg alfentanil and group 4 received 5 micrograms/kg fentanyl one minute before induction. Suxamethonium was given 60 seconds after induction and intubation of the trachea was performed 150 seconds after the start of induction. Heart rate and mean arterial pressure were recorded every minute throughout and compared with pre-induction control values. Control patients (group 1) showed significant increases associated with tracheal intubation in all haemodynamic variables. No increases were noted in groups receiving 30 micrograms/kg alfentanil or 5 micrograms/kg fentanyl. The heart rate, but not blood pressure, increased with intubation after 15 micrograms/kg alfentanil. The mean time to movement in 50% of the control patients was 7 minutes. In those given 15 and 30 micrograms/kg alfentanil it was 11 and 12 minutes respectively. In those given 5 micrograms/kg fentanyl it was greater than 15 minutes. Alfentanil is shown to reduce the cardiovascular responses to laryngoscopy and intubation and the effect appears to have a shorter duration than that of fentanyl.