Effect of esmolol on hemodynamics and intraocular pressure response to succinylcholine and intubation following low-dose alfentanil premedication.

STUDY OBJECTIVE: To determine the effectiveness of esmolol hydrochloride (Brevibloc) as an additional adjunct to low-dose alfentanil premedication in controlling the hemodynamic response [heart rate (HR), mean arterial pressure (MAP), and intraocular pressure (IOP)] to succinylcholine and endotracheal intubation. DESIGN: Randomized, double-blind, placebo-controlled, prospective study. SETTING: Ambulatory gynecologic surgery at a university medical center. PATIENTS: Twenty ASA physical status I and II female patients scheduled for outpatient laparoscopy under general anesthesia. INTERVENTIONS: All patients received alfentanil 10 micrograms/kg as a preoperative medication 4 minutes prior to induction of anesthesia. Study patients (n = 10 in each group) received either esmolol 1.5 mg/kg or a placebo (normal saline) 30 seconds prior to induction (210 seconds after alfentanil and 90 seconds prior to endotracheal intubation). Anesthesia was induced with thiopental sodium 5 mg/kg and succinylcholine 1 mg/kg. Postintubation, 70% nitrous oxide, 30% oxygen, and 1% isoflurane were administered. MEASUREMENTS AND MAIN RESULTS: Time of study drug administration was defined as time zero. Measurements of HR, MAP, and IOP were made at baseline (patient awake) and at each minute from minutes 1 through 6 after administration of the study drug (time zero). Analysis of variance was used to analyze the data, with a value of p less than 0.05 considered significant. Esmolol 1.5 mg/kg was found to blunt the maximum increase in HR but not MAP or IOP following low-dose alfentanil premedication. CONCLUSIONS: In an eye patient with coronary artery disease, or in any patient in whom tachycardia may be detrimental, esmolol may be a useful adjunct in combination with low-dose alfentanil to attenuate the increase in HR due to laryngoscopy and endotracheal intubation.     

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.     

Attenuation of hemodynamic responses to rapid sequence induction and intubation in healthy patients with a single bolus of esmolol

The effectiveness of a single preinduction intravenous (IV) bolus of esmolol in blunting hemodynamic responses to rapid sequence induction and tracheal intubation was evaluated. In a randomized double-blind study, 32 ASA I and II healthy patients scheduled for surgery were monitored with electrocardiography (EKG) lead V5, arterial cannulation, and impedance cardiography. After preoxygenation and a priming dose of vecuronium (0.01 mg/kg), patients received either saline (n = 12), esmolol 100 mg (n = 10), or esmolol 200 mg (n = 10) as an IV bolus (20 ml volume). This procedure was immediately followed by a 5 ml IV saline flush, cricoid pressure, thiopental sodium 5 mg/kg, and succinylcholine 1.5 mg/kg. Patients receiving 200 mg of esmolol had a 50% reduction in the usual tachycardia associated with induction and a greater decline in systolic blood pressure (SP) (by 50%) prior to intubation as compared with the placebo group (p less than 0.05). The increase in diastolic blood pressure (DP) and the reduction in stroke volume (SV) produced by induction and intubation were similar in all the groups. Plasma norepinephrine levels at 1.5 minutes after intubation increased in the esmolol groups about 130% above that measured in the placebo group. This finding was associated with a more gradual return of peripheral resistance to baseline following tracheal intubation. However, both doses of esmolol effectively attenuated heart rate (HR), SP, and rate pressure product (RPP) increases (p less than 0.05 vs placebo) produced by laryngoscopy and tracheal intubation.     

Lack of effect of intravenous lidocaine on hemodynamic responses to rapid sequence induction of general anesthesia: a double-blind controlled clinical trial

A double-blind, randomized trial was conducted in 16 women aged 20-48 yr, to assess the effect of intravenous lidocaine on the circulatory responses to rapid sequence induction of general anesthesia. None of the patients suffered from heart or lung diseases, all were scheduled for hysterectomy, and all were premedicated with 0.3 mg/kg diazepam orally 2 hr beforehand. Induction, preceded by preoxygenation, included simultaneous injection of thiopental and succinylcholine, without starting manual ventilation until the airway was secured with the endotracheal tube. Two minutes before laryngoscopy and intubation half of the patients received lidocaine, 1.5 mg/kg, intravenously (IV). The other half received an equal volume of saline. Cuff blood pressure was measured repeatedly by an automatic recording device, and heart rate and left ventricular ejection fraction (LVEF) were monitored by a portable nonimaging nuclear probe. After laryngoscopy and intubation, mean blood pressure increased 46%, heart rate 57%, and the rate pressure product (RPP) 84% from control values in patients given lidocaine, compared to 45, 66, and 113%, respectively, in the saline group (P greater than 0.05). Pronounced, but similar decreases in LVEF were observed in the two groups, to 0.40 from 0.65 in the lidocaine group and to 0.41 from 0.65 in the saline group. In all patients, RPP reached a level considered potentially dangerous to patients with ischemic heart disease. We conclude that lidocaine, 1.5 mg/kg IV, 2 min prior to laryngoscopy and intubation does not prevent hemodynamic reactions evoked by rapid sequence induction.     

Anaesthetic induction with alfentanil: comparison with thiopental, midazolam, and etomidate

The speed, side effects and cardiovascular changes associated with anaesthetic induction and endotracheal intubation following alfentanil (20 micrograms/kg/min, IV), thiopental (84 micrograms/kg/min, IV), etomidate (5 micrograms/kg/min, IV) and midazolam (20 micrograms/kg/min, IV) prior to halothane-nitrous oxide general anaesthesia were evaluated and compared in 80 patients undergoing elective general surgical operations. Anaesthetic induction was fastest with etomidate and thiopental (approximately one minute) and slowest with midazolam (about two minutes). Systolic arterial blood pressure (SBP) was decreased at the moment of unconsciousness with thiopental but unchanged with the other compounds. Heart rate (HR) was increased at unconsciousness with midazolam and thiopental but unchanged with etomidate and alfentanil. After intubation HR was increased in all groups except those induced with alfentanil. Arrhythmias were infrequent (5 per cent or less in all groups). Rigidity during induction only occurred with alfentanil (55 per cent) and pain on injection only with etomidate (35 per cent) and alfentanil (5 per cent). Postoperative vomiting was infrequent in all groups (15 per cent) except etomidate (55 per cent). No patient remembered any aspect of laryngoscopy or the operation and all rapidly regained consciousness at the end of operation. The results of this study demonstrate that with the exception of rigidity (which is easily overcome with succinylcholine) and a slightly slower onset of action, alfentanil compares favourably as an induction agent with thiopental and is better than midazolam and etomidate. Alfentanil is superior to all three other induction agents with respect to cardiovascular stability during induction and intubation.     

Does alfentanil preserve left ventricular pump function during rapid sequence induction of anaesthesia?

A double-blind, randomised trial was conducted in 24 patients without cardiopulmonary disorders (20-43 years), to assess the effect of an intravenous bolus of alfentanil on the circulatory and catecholamine responses to rapid sequence induction of general anaesthesia. Induction included injection of thiopentone 5 mg/kg and suxamethonium 1.5 mg/kg in rapid succession, followed by laryngoscopy and intubation. Half of the patients received alfentanil 100 micrograms/kg immediately before thiopentone. The other half received saline. Blood pressure, heart rate, and plasma catecholamine concentrations were measured repeatedly, together with left ventricular ejection fraction assessed by radionuclide angiocardiography. The responses following laryngoscopy and intubation were completely different in the saline vs. the alfentanil group: rate pressure product +76% vs. -32%, mean arterial blood pressure +46% vs. -25%, heart +46% vs. no change, noradrenaline +117% vs. -25%, adrenaline +50% vs. -53%, and left ventricular ejection fraction -32% vs. no change. In conclusion, during rapid sequence induction of anaesthesia with thiopentone and suxamethonium, an intravenous bolus of alfentanil 100 micrograms/kg 1 min before laryngoscopy and intubation completely prevents hypertension, tachycardia, decrease in left ventricular ejection fraction, and activation of plasma catecholamines, though at the expense of moderate hypotension.     

Attenuation of hypertensive response to tracheal intubation with nitroglycerin.

STUDY OBJECTIVE: To evaluate the efficacy and safety of intravenous (IV) nitroglycerin in attenuating the hypertensive response to laryngoscopy and intubation as a new application of the drug. DESIGN: Controlled, randomized, double-blind study. SETTING: University hospital. PATIENTS: Thirty normotensive patients (ASA physical status I) undergoing elective surgery were divided into three groups of ten patients each. INTERVENTIONS: Anesthesia was induced with thiopental sodium 5 mg/kg i.v., and tracheal intubation was facilitated with vecuronium 0.2 mg/kg i.v. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Either 1.5 micrograms/kg of nitroglycerin, 2.5 micrograms/kg of nitroglycerin, or saline (control) was administered IV simultaneously with the start of laryngoscopy (lasting 30 seconds), which was attempted 2 minutes after administration of thiopental sodium and vecuronium. MEASUREMENTS AND MAIN RESULTS: Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in nitroglycerin-treated patients compared with those in the control group (p < 0.05). CONCLUSION: A single, rapid IV dose of nitroglycerin is a simple, practical, effective, and safe method to attenuate the hypertensive response to laryngoscopy and tracheal intubation.     

Cardiovascular response to tracheal intubation in patients with intracranial tumor. Comparative study between urapidil and lidocaine

OBJECTIVES: To compare the effects of urapidil and lidocaine on cardiovascular response to laryngoscopy and tracheal intubation in patients with brain tumors. PATIENTS AND METHODS: Prospective, randomized double-blind study of 40 ASA II-III patients undergoing elective surgery for supratentorial tumor resection. The patients were assigned to two groups of 20 to receive an intravenous bolus of 1.5 mg/kg of lidocaine or 0.4 mg/kg urapidil before laryngoscopy and intubation. Anesthetic induction was performed with 0.03 mg/kg midazolam, 3 micrograms/kg of fentanyl, 5 mg/kg of thiopental and 0.2 mg/kg of vecuronium. Anesthesia was maintained with N2O/O2 (60%/40%) and isoflurane (0.5% expired). The following variables were recorded: mean blood pressure, heart rate and arterial oxygen saturation (SpO2) at baseline and 1, 2 and 3 min after induction and at 1, 2, 3, 4, 5 and 10 min after laryngoscopy and tracheal intubation. RESULTS: The two groups were comparable with respect to age, sex, weight, height and baseline hemodynamics. No statistically significant differences in hemodynamic variables were found between the two groups. Mean blood pressure in the postintubation period stayed near baseline and heart rate increased significantly after laryngoscopy and tracheal intubation in both groups. SpO2 decreased 7 min after administration of urapidil and stayed lower throughout the study period and was statistically different from SpO2 in the lidocaine group. All changes described were within clinically normal ranges. CONCLUSIONS: In patients undergoing neurosurgery to remove a supratentorial tumor, both lidocaine and urapidil reduce the pressor response to laryngoscopy and tracheal intubation at the doses given in this study. However, neither was able to prevent the increase in heart rate.     

Effects of aerosolized and/or intravenous lidocaine on hemodynamic responses to laryngoscopy and intubation in outpatients

A randomized, double-blind study was carried out on 40 unpremedicated, ASA I-II adult surgical outpatients to assess the effects of aerosolized lidocaine, intravenous lidocaine, both, or neither, on circulatory responses to laryngoscopy and intubation. Lidocaine (4 mg/kg) or saline was given by nebulizer in the holding area beginning at -15 minutes. The patient underwent a standardized induction of anesthesia that included IV curare (3 mg) and O2 by facemask at minute 2, followed by IV thiopental (5 mg/kg) and succinylcholine (1.5 mg/kg) at minute 5. Lidocaine (2 mg/kg) or saline was given by IV push at minute 4. Laryngoscopy was begun at 5 minutes and continued for 45 seconds before intubation. Heart rate and systolic, diastolic, and mean blood pressures were automatically recorded at 1-minute intervals from 0 to 11 minutes. The four treatment groups included: group 1, aerosolized and IV saline; group 2, aerosolized saline, IV lidocaine; group 3, aerosolized lidocaine, IV saline; and group 4, aerosolized and IV lidocaine. There were no differences among the four treatment groups (n = ten per group) in any of the four hemodynamic variables before laryngoscopy and intubation. Within each group, after intubation all four hemodynamic variables increased significantly over the corresponding baseline values for that group. However, the maximum values attained after intubation did not differ significantly among the four treatment groups for any of the four hemodynamic variables, whether those maxima were expressed as absolute values or as a percentage of baseline.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alfentanil as an anesthetic induction agent--a comparison with thiopental-lidocaine

Alfentanil (0.175 mg/kg) and a combination of thiopental (3-4 mg/kg) and lidocaine (1.5 mg/kg) during anesthetic induction were compared. Each was administered rapidly to eight patients with cardiovascular disease (average age, 64 yr), followed by succinylcholine (1.5 mg/kg) for laryngoscopy and intubation. Chest wall rigidity or flexor spasm of arm and jaw were seen transiently in 7 of 8 patients receiving alfentanil. Both drugs led to decreases in mean arterial pressure averaging 31 mm Hg (P less than 0.01). In patients given thiopental-lidocaine, intubation led to a 28 mm Hg (P less than 0.01) increase over control in arterial pressure and a 10 beats . min-1 increase in heart rate (P less than 0.01). In patients given alfentanil, after intubation arterial pressure returned to levels no different from control and the heart rate remained stable. Five of the patients given alfentanil required a single dose of naloxone (0.08-0.15 mg) to achieve a PCO2 less than 50 torr at the end of surgery. Rapidly administered alfentanil blunted the cardiovascular response to intubation but decreased arterial pressure as much as thiopental-lidocaine.     

Facilitation of fiberoptic nasotracheal intubation by simultaneous direct laryngoscopy in anesthetized patients

Two cases of unexpected difficult intubation during induction of general anesthesia were reported. The first case, a 68-year-old male was scheduled for coronary artery bypass surgery. The second case, a 94-year-old male with senile dementia was arranged for exploratory laparotomy. Anesthesia was induced with diazepam 10 mg, fentanyl 30 micrograms/kg, and pancuronium 8 mg in the first case while in the second case fentanyl 100 micrograms, lidocaine 80 mg, thiopental 200 mg and succinylcholine 80 mg were used. In these two cases oral tracheal intubation with laryngoscope was unsuccessful. Assisted ventilation could be maintained via a face mask. With the help of direct laryngoscopy, fiberoptic bronchoscope-aided nasotracheal intubation was successfully achieved.     

QT interval of the ECG, heart rate and arterial pressure during anaesthetic induction: comparative effects of alfentanil and esmolol

In a double-blind study the effect of esmolol and alfentanil on the QT interval of the ECG corrected by the heart rate (QTc), heart rate and arterial pressure during anaesthetic induction was studied in 59 oxycodone- and atropine-premedicated ASA class I-(II) patients with a mean age of 26 yr (range 15–50 yr). The patients were randomly allocated to one of the four groups: saline, esmolol 2 mg · kg^-1, esmolol 3 mg · kg^-1 or alfentanil 0.03 mg·kg^-1. Both doses of esmolol prevented the prolongation of the QTc interval after thiopental and suxamethonium, but not after laryngoscopy and intubation. Alfentanil prevented the prolongation of the QTc interval following thiopental, suxamethonium and laryngoscopy but not after intubation. Esmolol did not prevent the increase in the heart rate and arterial pressure in response to laryngoscopy and intubation. No cardiovascular responses to laryngoscopy and intubation occurred in the patients treated with alfentanil. No cardiac arrhythmias occurred in the esmolol 3 mg·kg^-1 group, whereas the frequency of ventricular ectopic beats was 40% in the saline group and 13–20% m the other groups.     

Effect of an intravenous nitroglycerin bolus on the hemodynamic impact of laryngoscopy and intubation]

The aim of this study was to evaluate the effectiveness of intravenous administration of a single dose of nitroglycerin in lessening the hemodynamic effects induced during laryngoscopy and tracheal intubation. In an initial subset of 8 patients we verified that the hemodynamic changes after an intravenous dose of 2, 5, or 10 micrograms/kg of nitroglycerin were comparable. The study included 30 patients with a good clinical condition who were anesthetized with fentanyl, thiopental sodium and succinylcholine. They were allocated into two groups of 15 patients according to the intravenous administration or not of 2 micrograms/kg of nitroglycerin after induction of anesthesia. Increase in systolic blood pressure (SBP) and double product (SBP x heart rate) during laryngoscopy and 15, 30, and 45 seconds thereafter was significantly lower in nitroglycerin treated patients than in controls. Increase in diastolic blood pressure was also lower in nitroglycerin treated patients but this difference was only present during laryngoscopy. There were no significant heart rate differences among the two groups of patients. It is concluded that a single intravenous dose of 2 micrograms/kg of nitroglycerin was able to lessen the increase in blood pressure induced by laryngoscopy and tracheal intubation without deleterious effects.     

Tracheal intubation without the use of muscle relaxants: a technique using propofol and varying doses of alfentanil.

We have noted that tracheal intubation can be accomplished in many patients after induction of anesthesia with propofol and alfentanil without the simultaneous use of muscle relaxants. This study was designed to evaluate airway and intubating conditions after administration of propofol and alfentanil in 75 ASA physical status I or II outpatients with Mallampati class I airways undergoing various surgical procedures. The patients were randomly assigned to one of five groups for induction of anesthesia. All patients received midazolam 1 mg IV before induction of anesthesia. Group I patients (n = 15) received d-tubocurarine 3 mg, thiamylal 4 mg/kg, and succinylcholine 1 mg/kg IV. Groups II-V patients (n = 15 each) received alfentanil 30, 40, 50, or 60 micrograms/kg followed by propofol 2 mg/kg IV. No muscle relaxants were given to patients in groups II-V. Airway management was performed by one of the authors who was blinded as to the dose of alfentanil administered. After loss of consciousness, patients' lungs were ventilated via face mask, and the ease of ventilation was recorded. Jaw mobility was also assessed. Ninety seconds after administration of the propofol or thiamylal, laryngoscopy was performed and exposure of the glottis and position of the vocal cords were noted. Intubation of the trachea was performed and patient response was noted. Heart rate and arterial blood pressure were also recorded before induction of anesthesia, after induction, and then again after intubation of the trachea. The lungs of all patients were easily ventilated via mask, and the jaw was judged to be relaxed in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lidocaine inhalation attenuates the circulatory response to laryngoscopy and endotracheal intubation.

STUDY OBJECTIVE: To evaluate the effect of lidocaine inhalation on the circulatory response to direct laryngoscopy and endotracheal intubation. DESIGN: Prospective, randomized study. SETTING: Operating theater at a public hospital. PATIENTS: Eighty patients (ASA physical status I and II ages 25 to 45 years) scheduled for major abdominal surgery. INTERVENTIONS: In the first stage, 40 patients were randomly assigned to receive inhalation of either lidocaine 40 mg or a 0.9% solution of sodium chloride (placebo). In the second stage, the next 20 consecutive patients received inhalation of lidocaine 120 mg, and another 20 consecutive patients received intravenous (IV) lidocaine 1 mg/kg. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure rose significantly in the i.v. lidocaine group (21.2 mmHg; p < 0.05), the saline inhalation group (29.2 mmHg; p < 0.05), and the lidocaine 40 mg inhalation group (22.9 mmHg; p < 0.05), but not in the lidocaine 120 mg inhalation group (10.1 mmHg). The heart rate (HR) response to intubation with lidocaine inhalation was dose dependent. In the saline inhalation group, HR increased by 15.6 beats per minute (bpm) (p < 0.05); in the lidocaine 40 mg inhalation group, HR increased by 9.1 bpm (p < 0.05); and in the lidocaine 120 mg inhalation group, HR increased by only 3.1 bpm. CONCLUSION: Inhalation of lidocaine 120 mg prior to induction of anesthesia is an effective, safe, and convenient method to attenuate the circulatory response to laryngoscopy and endotracheal intubation.     

Effects of combining midazolam and barbiturate on the response to tracheal intubation: changes in autonomic nervous system

STUDY OBJECTIVE: To investigate the effects on the autonomic nervous system of anesthesia induction with a combination of midazolam and barbiturate using plasma catecholamine concentration and heart rate (HR) variability in comparison with the induction with barbiturate alone. DESIGN: Prospective study. SETTING: Operating room of a university hospital. PATIENTS: 40 ASA physical status I and II patients aged 30 to 70 years, who were scheduled for general anesthesia. INTERVENTIONS: Anesthesia was induced with 0.1 mg/kg midazolam followed by 3 mg/kg thiopental sodium (Midazolam-Barbiturate group) or thiopental 5 mg/kg (Barbiturate group) with 6 L/min oxygen. MEASUREMENTS: Arterial blood pressure (BP), HR, HR variability, and plasma concentrations of epinephrine and norepinephrine were measured. MAIN RESULTS: Blood pressure and HR increased in response to tracheal intubation in both groups, but the increase was significantly larger in the Barbiturate group. In the Barbiturate group, the high-frequency component (HF) in HR variability increased significantly during intubation, whereas in the Midazolam-Barbiturate group, HF decreased continuously. The low-frequency component (LF)/HF ratio increased in both groups, with significantly higher values noted in the Barbiturate group. Plasma epinephrine concentrations decreased before intubation and increased in response to tracheal intubation in the Barbiturate group. Finally, plasma norepinephrine concentrations increased in response to tracheal intubation only in the Barbiturate group. CONCLUSIONS: Anesthesia induction with a combination of midazolam-thiopental was effective in reducing hemodynamic and cardiac autonomic nervous system responses to tracheal intubation in comparison with the conventional induction with thiopental alone.     

Effect of buprenorphine on the cardiovascular response to tracheal intubation

The effects of buprenorphine on the haemodynamic responses to tracheal intubation were studied in a placebo-controlled double-blind trial in 40 patients who had elective surgery. In one group saline was administered intravenously 8 minutes before induction, whereas the others received buprenorphine 2.5 micrograms/kg intravenously. Anaesthesia was induced in both groups with thiopentone 4 mg/kg followed by suxamethonium 1.5 mg/kg after 90 seconds. In the buprenorphine group, the maximum increase in systolic and diastolic arterial blood pressures, heart rate and rate pressure product were significantly lower compared to the control group. It is concluded that buprenorphine is partially effective in attenuating the cardiovascular response to laryngoscopy and intubation, but does not obliterate it.     

The effect of lidocaine on neutrophil respiratory burst during induction of general anaesthesia and tracheal intubation

BACKGROUND AND OBJECTIVE: Respiratory burst is an essential component of the neutrophil's biocidal function. In vitro, sodium thiopental, isoflurane and lidocaine each inhibit neutrophil respiratory burst. The objectives of this study were (a) to determine the effect of a standard clinical induction/tracheal intubation sequence on neutrophil respiratory burst and (b) to determine the effect of intravenous lidocaine administration during induction of anaesthesia on neutrophil respiratory burst. METHODS: Twenty ASA I and II patients, aged 18-60 years, undergoing elective surgery were studied. After induction of anaesthesia [fentanyl (2 microg kg-1), thiopental (4-6 mg kg-1), isoflurane (end-tidal concentration 0.5-1.5%) in nitrous oxide (66%) and oxygen], patients randomly received either lidocaine 1.5 mg kg-1 (group L) or 0.9% saline (group S) prior to tracheal intubation. Neutrophil respiratory burst was measured immediately prior to induction of anaesthesia, immediately before and 1 and 5 min after lidocaine/saline. RESULTS: Neutrophil respiratory burst decreased significantly after induction of anaesthesia in both groups [87.4 +/- 8.2% (group L) and 88.5 +/- 13.4% (group S) of preinduction level (P < 0.01 both groups)]. After intravenous lidocaine (but not saline) administration, neutrophil respiratory burst returned towards preinduction levels, both before (97.1 +/- 23.6%) and after (94.4 +/- 16.6%) tracheal intubation. CONCLUSION: Induction of anaesthesia and tracheal intubation using thiopentone and isoflurane, inhibit neutrophil respiratory burst. This effect may be diminished by the administration of lidocaine.     

Partial attenuation of the cardiovascular responses to tracheal intubation with oral nisoldipine.

STUDY OBJECTIVE: To evaluate the efficacy and safety of nisoldipine given orally in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: Induction of anesthesia for elective surgery at a university hospital. PATIENTS: Thirty normotensive patients (ASA physical status I) undergoing elective surgery were assigned to one of three groups; placebo, nisoldipine 5 mg, or nisoldipine 10 mg. Each group consisted of ten patients. INTERVENTIONS: Either 5 mg of nisoldipine, 10 mg of nisoldipine, or a placebo was administered orally 2 hours 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 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 associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in patients receiving nisoldipine 10 mg compared with patients receiving the placebo (p less than 0.05). CONCLUSIONS: Oral administration of nisoldipine before induction of anesthesia is a simple, practical, and safe method for attenuating pressor response to laryngoscopy and tracheal intubation.     

Partial attenuation of hemodynamic responses to rapid sequence induction and intubation with labetalol

The effectiveness of labetalol (a combination nonselective beta and alpha-1-adrenergic receptor antagonist) in modifying hemodynamic responses associated with rapid sequence induction and tracheal intubation was evaluated. In a double-blind study, 24 ASA physical status I or II male patients scheduled for elective surgery were given either IV labetalol, 0.25 mg/kg (n = 8) or 0.75 mg/kg (n = 8), or a saline placebo (n = 8). Five minutes later, patients were given oxygen by mask and IV vecuronium, 0.01 mglkg. Ten minutes after giving labetalol or placebo, cricoid pressure was applied and anesthesia was induced with IV sodium thiopental (4 mg/kg) and succinylcholine (1.5 mg/kg) 1 minute prior to intubation. The mean duration of laryngoscopy was 17 ± 3 seconds. Prior to induction, the 0.25 mg/kg and 0.75 mg/kg) doses of labetalol significantly (p < 0.05) reduced mean arterial pressure by 4.4 ± 1.9 and by 8.6 ± 2.0 mmHg, respectively, but did not significantly alter heart rate or cardiac output. The 0.75 mg/kg) dose of labetalol also significantly (p < 0.05) decreased total peripheral resistance by 10.1 ± 3.0%. Within 30 seconds after intubation, patients in all three groups exhibited increases in heart rate, mean arterial pressure, total peripheral resistance, and rate pressure product and a decrease in stroke volume. However, patients in the 0.25 and 0.75 mg/kg) labetalol groups, compared to those in the placebo group, had significantly lower increases in peak heart rate (33 ± 2 and 27 ± 3 vs. 44 ± 7 beats/minute), peak mean arterial pressure (38 ± 6 and 38 ± 7 vs. 58 ± 7 mmHg), and peak rate pressure product (7,726 ± 260 and 7,215 ± 300 vs. 14,023 ± 250 units). The results show that these doses of labetalol significantly blunt, but do not completely block, autonomic responses to rapid sequence induction and intubation.