Reduction of the concentration of isoflurane prevents tachycardia and hypertension associated with tracheal intubation

BACKGROUND: High concentration of isoflurane often induces not only tachycardia but also hypertension during induction of anesthesia and causes further hyperdynamic changes after tracheal intubation. METHODS: Forty patients, ASA physical status I, were randomly assigned to receive 4% or 2.5% isoflurane. Anesthesia was induced with thiamylal and vecuronium followed by mask ventilation with 0.5% isoflurane in oxygen. Isoflurane concentration was gradually increased to 4% or 2.5% in 2 min and the trachea was intubated after 3 min. Systolic blood pressure (SBP) and heart rate (HR) were recorded every minute from induction of anesthesia. RESULTS: Mask ventilation with isoflurane induced a significant increase in HR in both groups, but the HR just before intubation was significantly lower in the 2.5% group than in the 4% group. SBP was significantly decreased in the 2.5% group, but a transient increase was seen in the 4% group. Tracheal intubation induced a marked increase in HR in both groups, but the HR was significantly lower in the 2.5% group than in the 4% group (115 +/- 14 and 130 +/- 18 beats x min(-1), respectively; P < 0.01). SBPs just after intubation were 166 +/- 24 and 154 +/- 20 mmHg in the 4% and 2.5% groups, respectively. The difference between the groups was not significant, but the patients in whom the SBP increased more than 180 mmHg were significantly fewer in the 2.5% group than in the 4% group (P < 0.05). CONCLUSIONS: Reduction of the isoflurane concentration from 4% to 2.5% during induction of anesthesia made the circulation stable, and decreased the incidence of excessive tachycardia and hypertension after tracheal intubation.     

Isoflurane in nitrous oxide and oxygen increases plasma concentrations of noradrenaline but attenuates the pressor response to intubation

The haemodynamic response to laryngoscopy and intubation was evaluated in 52 ASA I patients anaesthetized with thiopentone 4-6 mg.kg-1. Vecuronium 0.1 mg.kg-1, followed by 3 min mask ventilation with nitrous oxide in oxygen with (isoflurane group) or without (control group) 3% inspired isoflurane preceded tracheal intubation. In 21 of 52 patients, concentrations of noradrenaline (NA), adrenaline and 3,4-dihydroxyphenylethyleneglycol (DHPG) were measured from central venous plasma. During the 3-min ventilation, in the isoflurane group, heart rate increased by 22% but remained stable in the control group. A marked pressor response to laryngoscopy and intubation was seen in the control but not in the isoflurane group. During the 3-min ventilation, the plasma concentration of NA was doubled in the isoflurane group and increased by 49% in the control group (P less than 0.05). The concentration of DHPG also increased in the isoflurane group. Peripheral skin temperature increased similarly after 3 min ventilation in both groups. After intubation, it was significantly higher in the isoflurane than in the control group (P less than 0.05). In conclusion, compared to nitrous oxide in oxygen, ventilation with isoflurane in nitrous oxide in oxygen causes a sympathetic activation combined with an increase in heart rate and peripheral temperature while the pressor response to laryngoscopy and intubation is attenuated.     

Effect of ONO-1101, a novel short-acting β-blocker on hemodynamic responses to isoflurane inhalation and tracheal intubation

Purpose We investigated the effect of a new ultrashort-acting β-blocker, ONO-1101, on hemodynamic responses to isoflurane inhalation and tracheal intubation. Methods Fifty-four ASA PS 1 or 2 patients were randomly allocated to receive either ONO-1101, 0.04 mg·kg⁻¹·min⁻¹, or saline prior to tracheal intubation. Anesthesia was induced with thiamylal, 4 mg·kg⁻¹, and vecuronium, 0.15 mg·kg⁻¹. Tracheal intubation was carried out after 3 min controlled mask ventilation with 66% N₂O and 3% inspired isoflurane in oxygen. Heart rate and blood pressure were continuously recorded from the start of induction until 5 min after intubation. Plasma concentrations of catecholamines were measured before induction, 3 min after initiating inhalation of isoflurane, and 1 min after tracheal intubation. Results Significant increases in heart rate occurred in both groups in response to isoflurane inhalation and tracheal intubation, but the magnitude of the increase was significantly less in the ONO-1101 group. Blood pressure increased after tracheal intubation in the saline group but remained unchanged in the ONO-1101 group. Plasma concentrations of norepinephrine increased after induction and intubation in both groups, with no significant difference between the groups. Conclusion ONO-1101 infusion is effective for the attenuation of hemodynamic responses to isoflurane inhalation and tracheal intubation.     

Successful use of i-gel in three patients with difficult intubation and difficult ventilation

I report successful ventilation through the i-gel and tracheal intubation through it, in patients in whom both facemask ventilation and tracheal intubation were difficult. Case 1: A 54-year-old woman, 157 cm, 60 kg, was scheduled for laparoscopic cholecystectomy. Preoperatively, neither difficult intubation nor difficult mask ventilation was predicted. After induction of anesthesia and neuromuscular blockade, both tracheal intubation and facemask ventilation were difficult. Insertion of a size 3 i-gel allowed adequate ventilation. The i-gel was removed and tracheal intubation was achieved using the Airway Scope. Case 2: In a 32-year-old woman, 162 cm, 46 kg, with predicted difficult intubation (thyromental distance of 4 cm), both tracheal intubation and facemask ventilation were difficult after induction of anesthesia. Insertion of a size 3 i-gel allowed adequate ventilation. Tracheal intubation through the i-gel was successful with the aid of a fibreoptic bronchoscope. Case 3: In a 54-year-old woman, 157 cm, 60 kg, with predicted difficult intubation (thyromental distance of 5 cm), both tracheal intubation and facemask ventilation were difficult after induction of anesthesia. Insertion of a size 3 i-gel allowed adequate ventilation. Fiberoptic tracheal intubation through the i-gel was successful. I feel that the i-gel has a potential role as a rescue device, by allowing ventilation and tracheal intubation in patients with difficult airways.     

Mask anesthesia for cerebral angiography in childhood moyamoya disease

Cerebral angiography is performed for diagnosis and management of moyamoya disease and in childhood moyamoya disease is usually carried out under general anesthesia after tracheal intubation. Mechanical irritation to trachea resulting in pain,cough,and increase in secretion after termination of the general anesthesia sometimes occurs and it sometimes causes hyperventilation resulting in hypocapnea. Continuous hypocapnea sometimes causes appearance of ischemic attacks in moyamoya disease. In the present study, we examine cerebral angiography conducted under general anesthesia using face mask ventilation in fourteen children with moyamoya disease. Sevoflurane was used as inhalation anesthetics. Face mask anesthesia was sixteen times in total in the 14 patients. Cerebral angiography terminated uneventfully in these patients except one patient who showed bronchospasm after induction of anesthesia and required tracheal intubation. However, the patient showed uneventful course after termination of the angiography. Tracheal irritation did not appear and all the patients were asleep just after termination of face mask anesthesia except for the patient who required tracheal intubation. In the latter case, the patient frequently coughed out phlegm after general anesthesia with tracheal intubation. In conclusion, general anesthesia with face mask ventilation was thought to be one of the suitable anesthetic methods introduced for cerebral angiography in childhood moyamoya disease.     

Anesthesia and hypertension: the effect of clonidine on perioperative hemodynamics and isoflurane requirements

Thirty patients (ASA physical status II-III) with a history of arterial hypertension, whose blood pressure (BP) control varied from normotension to moderate hypertension (diastolic BP less than 110 mmHg), scheduled for elective surgery under general anesthesia, were randomly assigned to two groups. Group 1 was premedicated 90-120 min prior to induction with diazepam 0.15 mg X kg-1 po; group 2, in addition, received clonidine 5 micrograms X kg-1 po. Anesthetic depth was assessed by on-line aperiodic analysis of the electroencephalogram. Following lidocaine 1 mg X kg-1 and fentanyl 2 micrograms X kg-1 (group 1 only), anesthesia was induced with thiopental 3-4 mg X kg-1 and vecuronium 0.1 mg X kg-1 was used to facilitate endotracheal intubation. Anesthesia was maintained with isoflurane in N2O/O2 and supplemented by fentanyl. In group 2, clonidine produced a rapid preoperative control of systolic and diastolic BP from 166 +/- 32/95 +/- 14 to 136 +/- 80 +/- 11 (P less than 0.01), was more effective in blunting the reflex tachycardia associated with laryngoscopy and endotracheal intubation than lidocaine-fentanyl pretreatment. It significantly reduced the intraoperative lability (coefficient of variation) of systolic (P less than 0.01) and diastolic BP and heart rate (HR) (P less than 0.05), and resulted in significantly slower HR during recovery (P less than 0.01). Anesthetic requirements for isoflurane were reduced 40% (P less than 0.01) in group 2; narcotic supplementation was also significantly reduced (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prevention of atelectasis formation during induction of general anesthesia

General anesthesia promotes atelectasis formation, which is augmented by administration of large oxygen concentrations. We studied the efficacy of positive end-expiratory pressure (PEEP) application during the induction of general anesthesia (fraction of inspired oxygen [FIO(2)] 1.0) to prevent atelectasis. Sixteen adult patients were randomly assigned to one of two groups. Both groups breathed 100% O(2) for 5 min and, after a general anesthesia induction, mechanical ventilation via a face mask with a FIO(2) of 1.0 for another 5 min before endotracheal intubation. Patients in the first group (PEEP group) had continuous positive airway pressure (CPAP) (6 cm H(2)O) and mechanical ventilation via a face mask with a PEEP of 6 cm H(2)O. No CPAP or PEEP was applied in the control group. Atelectasis, determined by computed radiograph tomography, and analysis of blood gases were measured twice: before the beginning of anesthesia and directly after the intubation. There was no difference between groups before the anesthesia induction. After endotracheal intubation, patients in the control group showed an increase of the mean area of atelectasis from 0.8% +/- 0.9% to 4.1% +/- 2.0% (P = 0.0002), whereas the patients of the PEEP group showed no change (0.5% +/- 0.6% versus 0.4% +/- 0.7%). After the intubation with a FIO(2) of 1.0, PaO(2) was significantly higher in the PEEP group than in the control (591 +/- 54 mm Hg versus 457 +/- 99 mm Hg; P = 0.005). Atelectasis formation is prevented by application of PEEP during the anesthesia induction despite the use of large oxygen concentrations, resulting in improved oxygenation. IMPLICATIONS: Application of positive end-expiratory pressure during the induction of general anesthesia prevents atelectasis formation. Furthermore, it improves oxygenation and probably increases the margin of safety before intubation. Therefore, this technique should be considered for all anesthesia induction, at least in patients at risk of difficult airway management during the anesthesia induction.     

Nitrous oxide induces paradoxical electroencephalographic changes after tracheal intubation during isoflurane and sevoflurane anesthesia

In this randomized, double-blind, controlled study, we tested the hypothesis that nitrous oxide (N2O) affects bispectral index (BIS) and 95% spectral edge frequency (SEF95) in response to tracheal intubation during anesthesia with isoflurane and sevoflurane. In protocol 1, we randomly allocated 90 ASA physical status I patients to 6 groups (n = 15 each). Anesthesia was induced with isoflurane or sevoflurane with 0%, 33%, or 66% N2O. The concentration of isoflurane and sevoflurane was gradually increased and end-tidal concentrations were maintained at 1.1% and 1.7%, respectively. Tracheal intubation was performed 12 min after induction of anesthesia. BIS was significantly increased 1 min after tracheal intubation compared before laryngoscopy in patients receiving only isoflurane or sevoflurane (P = 0.001 and 0.007, respectively). In patients receiving 66% N2O-isoflurane or 66% N2O-sevoflurane, both BIS and SEF95 were significantly decreased after tracheal intubation and significantly lower than in those patients receiving only isoflurane or sevoflurane, respectively (P < 0.01 for both). In protocol 2, 3 microg/kg of IV fentanyl completely abolished the decrease of BIS and SEF95 after tracheal intubation during anesthesia with 66% N2O-isoflurane and 66% N2O-sevoflurane (n = 10). We conclude that 66% N2O induced a paradoxical decrease of BIS in response to tracheal intubation during anesthesia with isoflurane and sevoflurane.     

Endotracheal administration of lidocaine inhibits isofluraneinduced tachycardia

PURPOSE: Rapid increase in inspired isoflurane concentration increases heart rate and arterial blood pressure. To investigate whether the responses to isoflurane were elicited from stimulation of lower airway and/or lungs, haemodynamic responses to isoflurane administered after tracheal intubation were measured with or without endotracheal or intravenous administration of lidocaine. METHODS: Seventy-two ASA physical status 1 patients, aged 21-50 yr, were randomly allocated to one of four groups. After tracheal intubation, anaesthesia was maintained with oxygen 100% and isoflurane 1.0% with controlled ventilation. After stabilization for 15 min, the isoflurane concentration was rapidly increased to 3.0% in three groups. An endotracheal lidocaine group received pretreatment with endotracheal 0.4 ml lidocaine 8% spray, an intravenous lidocaine group received pretreatment of 32 mg lidocaine i.v., and an isoflurane 3% group received not pre- treatment. In a control group, inspired isoflurane concentration was maintained at 1.0%. Heart rate, systolic blood pressure and end-tidal isoflurane concentration were measured every minute for 10 min. RESULTS: The rapid increase in isoflurane concentration increased heart rate (25 +/- 12% increase from baseline; P < 0.05) but the increase was reduced by endotracheal lidocaine (9 +/- 9%), but not by intravenous lidocaine (22 +/- 13%). The plasma concentration of lidocaine was lower in the endotracheal lidocaine group (0.4 +/- 0.3 microgram.ml-1) than in the i.v. lidocaine group (1.5 +/- 0.2 micrograms.ml-1). CONCLUSION: The isoflurane-induced tachycardia is reduced by pre-treatment with endotracheal lidocaine.     

Airway management in a patient with Williams syndrome

Williams syndrome is characterized by the triad of supravalvular aortic stenosis (SAS), mental retardation and elfin facies. Generally, difficult airway is expected in patients with Williams syndrome by characteristic face. A 26-year-old female with Williams syndrome was scheduled for abdominal myomectomy under general anesthesia. Difficult mask ventilation and tracheal intubation were anticipated because of micrognathia, mandibular retrusion, and a Mallanpati class III airway. Before induction of anesthesia the patient breathed 100% oxygen for 3 minutes. Anesthesia was induced and maintained with propofol, remifentanil and rocuronium bromide. Mask ventilation was easily performed. The direct laryngoscopic view was Cormack grade I and there was no difficulty in the tracheal intubation. After induction of anesthesia, anesthetic course was uneventful. According to the most previous clinical reports in patients with Williams syndrome in Japan, mask ventilation and tracheal intubation were performed easily contrary to preoperative airway assessment. In view of SAS, mental retardation, airway deformity and airway assessment in previous clinical reports, we should select the optimal strategy for airway management in patients with Williams syndrome.     

Fiberoptic intubation in adult patients with predictive signs of difficult intubation: inhalational induction using sevoflurane and an endoscopic facial mask

OBJECTIVE: To evaluate the combination of inhalational induction with sevoflurane and fiberoptic intubation through a specific facial mask for anticipated difficult tracheal intubation (DI) in adults. STUDY DESIGN: Prospective study. PATIENTS AND METHODS: Eighteen consecutive patients at risk of DI. After premedication made of hydroxyzine 2 mg x kg(-1), preoxygenation, 0.1 microg x kg(-1) sufentanil was administered (T0), then, inhalational induction was started: sevoflurane 8% in 100% O2 l x min(-1). After 1 min, sevoflurane was decreased to 5% and, if necessary, adapted to obtain an adequate depth of anaesthesia (Ramsay score > 3). Fiberoptic bronchoscopy was performed through a Fibroxy mask. BP was measured every 2.5 min, HR, SpO2, RR were recorded. The results were analyzed by Newman-Keuls test. RESULTS: Intubation was easily realized but it was necessary to assist ventilation in patients presenting prolonged apnea lasting more than 30 s (5 out of 9 patients who presented apnea during procedure). Intubation was quickly realized (T+ 4 +/- 3 min). Haemodynamics and saturation were not altered during procedure. Inhalatory induction using sevoflurane costs 6 10 versus 16 80 for intravenous target controlled propofol anesthesia (using only one preconditionned syringe). CONCLUSION: Inhalational induction with sevoflurane and fiberoptic intubation appeared easy, fast and cheap.     

Effects of nilvadipine on the cardiovascular responses to tracheal intubation.

STUDY OBJECTIVE: To evaluate the efficacy of nilvadipine given orally in attenuating the hypertensive response to laryngoscopy and intubation. DESIGN: Controlled, randomized, double-blind study. SETTING: Induction of anesthesia for elective surgery at a university hospital. PATIENTS: Thirty normotensive patients (ASA physical status I) undergoing elective surgery were divided into three groups of ten patients each. INTERVENTIONS: Either 2 mg of nilvadipine, 4 mg of nilvadipine, or a placebo (control) was administered orally 90 minutes before induction of anesthesia. Anesthesia was induced with thiopental sodium 5 mg/kg intravenously, and tracheal intubation was facilitated with vecuronium 0.2 mg/kg. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide (N2O) in oxygen. Laryngoscopy lasting 30 seconds was attempted 2 minutes after administration of thiopental sodium and vecuronium. MEASUREMENTS AND MAIN RESULTS: Patients receiving the placebo showed a significant increase in mean arterial pressure (MAP) and heart rate associated with tracheal intubation. The increase in MAP following tracheal intubation was significantly lower in nilvadipine-treated patients than in the control group (p less than 0.05). However, neither dose of nilvadipine attenuated the tachycardic response to intubation. CONCLUSIONS: Oral administration of nilvadipine before induction of anesthesia is a simple and practical method for attenuating pressor response to laryngoscopy and tracheal intubation after standard elective induction under additional 1% enflurane-N2O anesthesia.     

Respiratory mechanics during sevoflurane anesthesia in children with and without asthma.

We studied lung function in children with and without asthma receiving anesthesia with sevoflurane. Fifty-two children had anesthesia induced with sevoflurane (up to 8%) in a mixture of 50% nitrous oxide in oxygen and then maintained at 3% with children breathing spontaneously via face mask and Jackson-Rees modification of the T-piece. Airway opening pressure and flow were then measured. After insertion of an oral endotracheal tube under 5% sevoflurane, measurements were repeated at 3%, as well as after increasing to 4.2%. Respiratory system resistance (Rrs) and compliance during expiration were calculated using multilinear regression analysis of airway opening pressure and flow, assuming a single-compartment model. Data from 44 children were analyzed (22 asthmatics and 22 normal children). The two groups were comparable with respect to age, weight, ventilation variables, and baseline respiratory mechanics. Intubation was associated with a significant increase in Rrs in asthmatics (17% +/- 49%), whereas in normal children, Rrs slightly decreased (-4% +/- 39%). At 4.2%, Rrs decreased slightly in both groups with almost no change in compliance system resistance. We concluded that in children with mild to moderate asthma, endotracheal intubation during sevoflurane anesthesia was associated with increase in Rrs that was not seen in nonasthmatic children. IMPLICATIONS: Tracheal intubation using sevoflurane as sole anesthetic is possible and its frequency is increasing. When comparing children with and without asthma, tracheal intubation under sevoflurane was associated with an increase in respiratory system resistance in asthmatic children. However, no apparent clinical adverse event was observed.     

Endotracheal Intubation, but Not Laryngeal Mask Airway Insertion, Produces Reversible Bronchoconstriction

Background: Tracheal intubation frequently results in an increase in respiratory system resistance that can be reversed by inhaled bronchodilators. The authors hypothesized that insertion of a laryngeal mask airway would be less likely to result in reversible bronchoconstriction than would insertion of an endotracheal tube.

Methods: Fifty-two (45 men, 7 women) patients were randomized to receive a 7.5-mm (women) or 8-mm (men) endotracheal tube or a No. 4 (women) or No. 5 (men) laryngeal mask airway. Anesthesia was induced with 2 [micro sign]g/kg fentanyl and 5 mg/kg thiopental, and airway placement was facilitated with 1 mg/kg succinylcholine. When a seal to more than 20 cm water was verified, respiratory system resistance was measured immediately after airway placement. Inhalation anesthesia was begun with isoflurane to achieve an end-tidal concentration of 1% for 10 min. Respiratory system resistance was measured again during identical conditions.

Results: Among patients receiving laryngeal mask airways, the initial respiratory system resistance was significantly less than among patients with endotracheal tubes (9.2 +/- 3.3 cm water [middle dot] 1-1 [middle dot] s (-1) [mean +/- SD] compared with 13.4 +/- 9.6 cm water [middle dot] 1-1 [middle dot] s-1; P < 0.05). After 10 min of isoflurane, the resistance decreased to 8.6 +/- 3.6 cm water [middle dot] 1-1 [middle dot] s-1 in the endotracheal tube group but remained unchanged at 9.1 +/- 3.3 cm water [middle dot] 1-1 [middle dot] s-1 in the laryngeal mask airway group. The decrease in respiratory system resistance in the endotracheal tube group of 4.7 +/- 7 cm water [middle dot] 1-1 [middle dot] s-1 was highly significant compared with the lack of change in the laryngeal mask airway group (P < 0.01).     

Blood pressure and heart rate changes during fibreoptic orotracheal intubation: a comparison of children and adults

BACKGROUND AND OBJECTIVES: Autonomic circulatory regulation and airway anatomy in children are significantly different from those in adults. There is no available published data to compare whether there is a clinically relevant difference in the haemodynamic responses to fibreoptic orotracheal intubation (FOI) under the same conditions between children and adults. In this randomized clinical study, we compared the blood pressure (BP) and heart rate (HR) changes during FOI in 40 children aged 3.5-9 yr and 40 adults aged 21-57 yr, ASA 1 scheduled for elective plastic surgery under general anaesthesia requiring orotracheal intubation. METHODS: Anaesthesia was induced with intravenous (i.v.) injection of fentanyl and propofol, and face mask inhalation of isoflurane before FOI. Noninvasive BP and HR were recorded before induction (baseline values), after induction (postinduction values), at intubation and for 5 min after intubation at 1-min intervals. The percentage changes of BP and HR at each time point were calculated. RESULTS: In children and adults, HR at intubation and 1-3 min after intubation were significantly higher than baseline and postinduction values. In adults, BP at intubation increased significantly compared to the postinduction values but did not exceed baseline values. In children, BP at intubation and 1 min after intubation were significantly higher than postinduction and baseline values. As compared to adults, FOI caused a more significant pressor response in children. The percentage changes of BP at intubation and 1 min after intubation were larger in children than in adults. However, there was no significant difference in the percentage change of HR during the observation between children and adults. CONCLUSIONS: Under general anaesthesia, FOI might cause a more significant pressor response in children than in adults.     

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.     

Fentanyl pretreatment attenuates the haemodynamic response to sudden inhalation of 5% isoflurane

High concentrations of inhaled isoflurane can increase heart rate and/or arterial pressure. The purpose of this study was to determine whether fentanyl has a prophylactic effect on the isoflurane-induced circulatory response in adult patients. Thirty patients due to undergo elective surgery were randomly allocated to one of three groups of ten patients. Prior to surgery, one group inhaled 2.5% isoflurane, another inhaled 5.0% isoflurane, and the third group inhaled 5.0% isoflurane and were given fentanyl 2 μg · kg^?1 iv two minutes before induction of anaesthesia. Anaesthesia was induced with thiamylal followed by vecuronium. The lungs were ventilated with 100% oxygen and either 2.5% or 5.0% isoflurane via face mask. Ventilation was continued for five minutes. Heart rate (HR) and mean arterial pressure (MAP) were recorded at two minutes before induction of anaesthesia (baseline), immediately before the induction of anaesthesia, and at three and five minutes after induction, respectively. It was found that 5.0% isoflurane caused an increase in HR compared with baseline (P < 0.01) and with the 2.5% isoflurane (P < 0.05): 2.5% isoflurane did not elicit this response. An increase was also noted in MAP, compared with the 2.5% isoflurane (P < 0.01): 2.5% isoflurane did not elicit this increase. Fentanyl pretreatment attenuated the increases in HR and in MAP that occurred with 5.0% isoflurane (P < 0.01). These results suggest that fentanyl attenuates the enhancement of both HR and MAP from face mask inhalation of a high concentration of isoflurane.     

The additive contribution of nitrous oxide to isoflurane MAC in infants and children

The purpose of this study was to determine the contribution of nitrous oxide to isoflurane MAC in pediatric patients. MAC was determined in 47 infants and small children (mean ages 16.6 +/- 6.7 months) during isoflurane and oxygen anesthesia (n = 11) and isoflurane and nitrous oxide anesthesia (25% nitrous oxide [n = 12], 50% nitrous oxide [n = 12], and 75% nitrous oxide [n = 12]). After assigning patients to one of four groups, anesthesia was induced with increasing inspired concentrations of isoflurane in oxygen. After anesthetic induction and tracheal intubation, ventilation was controlled (carbon dioxide partial pressure = 32 +/- 5 mmHg), and nitrous oxide was added to the inspired gas mixture to achieve end-expired nitrous oxide concentrations of 0, 25, 50, or 75%. Inspired and expired gas samples were obtained from a distal sampling port in the tracheal tube. The response to skin incision in each patient was assessed at a previously selected end-tidal concentration of isoflurane. The MAC of isoflurane was determined in each group using the up-and-down method described for evaluating quantal responses. The mean duration of constant end-tidal concentrations prior to skin incision was 14 +/- 7 min (range 6-46 min). The ratio of expired to inspired nitrous oxide and isoflurane concentrations during the period of constant end-tidal concentrations was 0.96 +/- 0.01 and 0.93 +/- 0.03 respectively. The MAC of isoflurane in oxygen was 1.69 +/- 0.13 vol% (mean +/- standard deviation).(ABSTRACT TRUNCATED AT 250 WORDS)     

Stress response to tracheal intubation in patients undergoing coronary artery surgery: direct laryngoscopy versus an intubating laryngeal mask airway

OBJECTIVE: Stress response caused by endotracheal intubation may be harmful for the coronary or cerebral circulation of high-risk patients. This study evaluated the hypothesis that tracheal intubation via an intubating laryngeal mask airway is associated with less cardiovascular and endocrine stress response than the conventional technique using direct laryngoscopy. DESIGN: Randomized, patient-blinded trial. SETTING: University department (single center). PARTICIPANTS: Eighty-six patients undergoing elective coronary artery surgery. INTERVENTION: Tracheal intubation was performed via an intubating laryngeal mask or by conventional direct laryngoscopy after standardized induction of anesthesia. MEASUREMENTS AND MAIN RESULTS: Electrocardiogram with automatic ST-segment analysis and invasive measured blood pressure were recorded continuously and blood samples to analyze norepinephrine plasma levels were taken at 4 times. Catecholamine concentrations and the pressure-rate product were analyzed by using an analysis of variance for repeated measures. In both groups, the pressure-rate product (p = 0.003) and norepinephrine concentrations (p < 0.0001) significantly decreased after induction of anesthesia. However, the fall was more marked in the patients intubated via the laryngeal mask (p = 0.031) than in patients receiving direct laryngoscopy. There were neither signs of cardiac ischemia nor major adverse events during induction of anesthesia. CONCLUSIONS: Reduction of cardiovascular and endocrine stress response associated with endotracheal intubation is more pronounced when performed via the intubating laryngeal mask. Thus, this technique can be helpful in high-risk cardiac patients.     

Comparison of nicardipine, diltiazem and verapamil for controlling the cardiovascular responses to tracheal intubation

We have compared the efficacy of three calcium channel blockers, nicardipine, diltiazem and verapamil, in attenuating the cardiovascular responses to laryngoscopy and intubation in 60 normotensive patients (ASA I) undergoing rapid sequence induction of anaesthesia with thiopentone and fentanyl. We also examined whether or not these blockers inhibited catecholamine release induced by intubation. The patients were allocated to one of four groups (n = 15 for each): saline (control), nicardipine 30 micrograms kg-1, diltiazem 0.2 mg kg-1 or verapamil 0.1 mg kg-1. Verapamil and the three other drugs were administered 45 s and 60 s before the start of direct laryngoscopy, respectively, in a double-dummy design. Anaesthesia was induced with thiopentone 4 mg kg-1 i.v. and fentanyl 2 micrograms kg-1 i.v. Tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. During anaesthesia, ventilation was assisted or controlled with 1% isoflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 s was attempted 2 min after administration of thiopentone and vecuronium. Patients receiving saline exhibited significant increases in systolic and diastolic arterial pressures (AP), heart rate (HR) and plasma concentrations of catecholamines associated with tracheal intubation. The increase in AP was attenuated in patients treated with any calcium channel blocker. The greatest effect was elicited by verapamil, which attenuated the increase in HR, although nicardipine seemed to enhance tachycardia. All three drugs failed to suppress the increase in plasma catecholamine concentrations in response to tracheal intubation. These findings suggest that bolus injection of verapamil 0.1 mg kg-1 was a more effective method of controlling hypertension and tachycardia associated with intubation than diltiazem 0.2 mg kg-1 or nicardipine 30 micrograms kg-1, and that these prophylactic effects were not caused by inhibition of the catecholamine response.