A comparison of pretreatment regimens for minimizing the haemodynamic response to blind nasotracheal intubation

The authors determined the cardiovascular effects of blind nasotracheal intubation in four randomized groups of 25 patients each. After induction of anaesthesia with IV thiopentone 4 mg X kg-1, patients in group A received no pretreatment, while patients in group B received IV lidocaine 1.5 mg X kg-1. Three minutes before induction, patients in group C received 0.25 per cent phenylephrine nasal spray (0.2 mg in each nostril); those in group D received ten per cent lidocaine nasal spray (30 mg in each nostril). After intubation, mean arterial pressures (MAP) were highest in group B (IV lidocaine) patients (p less than 0.05), remaining significantly elevated for 5 min. Conversely, within four minutes after intubation, MAP of group D (ten per cent nasal lidocaine spray) patients were below control (p less than 0.05), and lower than those of any other group (p less than 0.05). MAP of group A and C patients increased after intubation, but not as much as in group B patients (p less than 0.05). There were no adverse effects from the lidocaine nasal spray. Ten per cent lidocaine nasal spray is a safe and effective way to minimize the MAP increases which typically accompany blind nasotracheal intubation in lightly anaesthetized patients.     

Cardiovascular responses to fiberoptic intubation: A comparison of orotracheal and nasotracheal intubation

We compared the cardiovascular responses between nasal and oral intubation with a fiberoptic bronchoscope under the combination of neuroleptic analgesia (NLA) and topical anesthesia. The 16 patients studied were divided into 2 groups: the nasal intubation group (N group: 8 patients) and the oral intubation group (O group: 8 patients). There were significant changes in systolic, diastolic and mean arterial pressures in the N group and in the pressure rate quotient in the O group. Diastolic arterial pressure and heart rate were significantly higher in the N group than in the O group before induction of general anesthesia. The rate pressure product (RPP) was significantly higher in the N group than in the O group at some points during the procedure. The individual RPP in both groups was relatively stable except for one patient in the N group, who had a marked increase in RPP during the procedure. We conclude that, under the combination of NLA and topical anesthesia, the cardiovascular responses to oral fiberoptic intubation are less severe than those to the nasal approach. The oral approach is recommended, especially in patients with coronary artery disease, taking into consideration of the cardiovascular responses to fiberoptic intubation.(Shibata Y, Okamoto K, Matsumoto M, et al.: Cardiovascular responses to fiberoptic intubation: a comparison of orotracheal and nasotracheal intubation. J Anesth 6: 262–268, 1992)     

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.     

氯普鲁卡因对经鼻气管插管心血管应激反应的影响

目的观察氯普鲁卡因与利多卡因对经鼻气管插管时血流动力学以及应激反应的影响。方法选择需经鼻气管插管行颌面手术患者45例,ASAⅠ或Ⅱ级,随机均分为三组,于气管插管前分别静注生理盐水(C组)、利多卡因1.5mg/kg(L组)和氯普鲁卡因3mg/kg(P组)。采用靶控输注丙泊酚(血浆浓度4μg/ml)全麻诱导及维持,静注0.1mg/kg维库溴铵4min后进行气管插管。监测插管前及插管后1、2、3和5min时的血流动力学变化,并测定血浆肾上腺素(E)及去甲肾上腺素NE)的含量。结果插管后1、2、3min,三组HR都明显增快,但P组明显慢于C组(P<0.05);P、组MAP显著低于C组(P<0.05);P、L组的E含量均显著低于C组(P<0.05),但两组间差异无统计学意义。插管后1minP组NE含量显著低于L组和C组(P<0.05)。插管后2、3minP、L组E含量均显著低于C组(P<0.05),但P、L两组间差异无统计学意义。结论经鼻气管插管前静脉注射3mg/kg氯普鲁卡因能有效减轻气管插管所致心血管应激反应。     

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).     

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.