Both Local Anesthetics and Salbutamol Pretreatment Affect Reflex Bronchoconstriction in Volunteers with Asthma undergoing Awake Fiberoptic Intubation

Background: Awake tracheal intubation may evoke reflex bronchoconstriction in asthmatics. Whether this effect is altered by the choice of the local anesthetic used or by pretreatment with a [beta]2-adrenoceptor agonist is unknown. Therefore, we assessed the effect of awake fiberoptic intubation after lidocaine or dyclonine inhalation with or without pretreatment with salbutamol on lung function in asthmatic volunteers.

Methods: Bronchial hyperreactivity was verified by an inhalational histamine challenge. On four different days in a randomized, double blind fashion the volunteers (n = 10) inhaled either dyclonine or lidocaine with or without salbutamol pretreatment. FEV1 was measured at baseline, following salbutamol or saline inhalation, after lidocaine or dyclonine inhalation, while intubated, and after extubation. Lidocaine and dyclonine plasma concentrations were also measured. Statistics: Two-way ANOVA, post hoc tests with Bonferroni correction, results are presented as mean +/- SD.

Results: Neither lidocaine nor dyclonine inhalation changed FEV1 significantly from baseline compared with placebo in-halation (4.43 +/- 0.67 l vs. 4.29 +/- 0.72 l, and 4.53 +/- 0.63 l vs. 4.24 +/- 0.80 l, respectively). Salbutamol slightly but significantly increased FEV1 (4.45 +/- 0.76 l vs. 4.71 +/- 0.61 l, P = 0.0034, and 4.48 +/- 0.62 l vs. 4.71 +/- 0.61 l, P = 0.0121, respectively). Following awake intubation FEV1 significantly decreased under lidocaine topical anesthesia (4.29 +/- 0.72 l to 2.86 +/- 0.87 l) but decreased even more under dyclonine anesthesia (4.24 +/- 0.80 l to 2.20 +/- 0.67 l;P < 0.0001). While salbutamol pretreatment significantly attenuated the response to intubation, it did not eliminate the difference between the effects of lidocaine and dyclonine. Only minutes after extubation FEV1 was similar compared with baseline.     

Airway Anesthesia Alone Does Not Explain Attenuation of Histamine-induced Bronchospasm by Local Anesthetics: A Comparison of Lidocaine, Ropivacaine, and Dyclonine

Background: Lidocaine inhalation attenuates histamine-induced bronchospasm while evoking airway anesthesia. Because this occurs at plasma concentrations much lower than those required for intravenous lidocaine to attenuate bronchial reactivity, this effect is likely related to topical airway anesthesia and presumably independent of the specific local anesthetic used. Therefore, the authors tested the effect of dyclonine, lidocaine, and ropivacaine inhalation on histamine-induced bronchospasm in 15 volunteers with bronchial hyperreactivity.

Methods: Bronchial hyperreactivity was verified by an inhalational histamine challenge. Histamine challenge was repeated after inhalation of dyclonine, lidocaine, ropivacaine, or placebo on 4 different days in a randomized, double-blind fashion. Lung function, bronchial hyperreactivity to histamine, duration of local anesthesia, and lidocaine and ropivacaine plasma concentrations were measured. Statistical analyses were performed with the Friedman and Wilcoxon rank tests. Data are presented as mean +/- SD.

Results: The inhaled histamine concentration necessary for a 20% decrease of forced expiratory volume in 1 s (PC20) was 7.0 +/- 5.0 mg/ml at the screening evaluation. Lidocaine and ropivacaine inhalation increased PC20 significantly to 16.1 +/- 12.9 and 16.5 +/- 13.6 mg/ml (P = 0.007), whereas inhalation of dyclonine and saline did not (9.1 +/- 8.4 and 6.1 +/- 5.0 mg/ml, P = 0.7268). Furthermore, in contrast to saline and lidocaine, inhalation of both ropivacaine and dyclonine significantly decreased forced expiratory volume in 1 s from baseline (P = 0.0016 and 0.0018, respectively). The longest lasting and most intense anesthesia developed after dyclonine inhalation (48 +/- 13 vs. 28 +/- 8 [lidocaine] and 25 +/- 4 min [ropivacaine]).     

Airway anesthesia alone does not explain attenuation of histamine-induced bronchospasm by local anesthetics: a comparison of lidocaine, ropivacaine, and dyclonine

BACKGROUND: Lidocaine inhalation attenuates histamine-induced bronchospasm while evoking airway anesthesia. Because this occurs at plasma concentrations much lower than those required for intravenous lidocaine to attenuate bronchial reactivity, this effect is likely related to topical airway anesthesia and presumably independent of the specific local anesthetic used. Therefore, the authors tested the effect of dyclonine, lidocaine, and ropivacaine inhalation on histamine-induced bronchospasm in 15 volunteers with bronchial hyperreactivity. METHODS: Bronchial hyperreactivity was verified by an inhalational histamine challenge. Histamine challenge was repeated after inhalation of dyclonine, lidocaine, ropivacaine, or placebo on 4 different days in a randomized, double-blind fashion. Lung function, bronchial hyperreactivity to histamine, duration of local anesthesia, and lidocaine and ropivacaine plasma concentrations were measured. Statistical analyses were performed with the Friedman and Wilcoxon rank tests. Data are presented as mean +/- SD. RESULTS: The inhaled histamine concentration necessary for a 20% decrease of forced expiratory volume in 1 s (PC20) was 7.0 +/- 5.0 mg/ml at the screening evaluation. Lidocaine and ropivacaine inhalation increased PC20 significantly to 16.1 +/- 12.9 and 16.5 +/- 13.6 mg/ml (P = 0.007), whereas inhalation of dyclonine and saline did not (9.1 +/- 8.4 and 6.1 +/- 5.0 mg/ml, P = 0.7268). Furthermore, in contrast to saline and lidocaine, inhalation of both ropivacaine and dyclonine significantly decreased forced expiratory volume in 1 s from baseline (P = 0.0016 and 0.0018, respectively). The longest lasting and most intense anesthesia developed after dyclonine inhalation (48 +/- 13 vs. 28 +/- 8 [lidocaine] and 25 +/- 4 min [ropivacaine]). CONCLUSION: Both lidocaine and the new amide local anesthetic ropivacaine significantly attenuate histamine-induced bronchospasm. In contrast, dyclonine, despite its longer lasting and more intense local anesthesia, does not alter histamine-evoked bronchoconstriction and irritates the airways. Thus, airway anesthesia alone does not necessarily attenuate bronchial hyperreactivity. Other properties of inhaled local anesthetics may be responsible for attenuation of bronchial hyperreactivity.     

Corticosteroids and inhaled salbutamol in patients with reversible airway obstruction markedly decrease the incidence of bronchospasm after tracheal intubation

BACKGROUND: In patients with bronchial hyperreactivity, airway instrumentation can evoke life-threatening bronchospasm. However, the best strategy for the prevention of bronchospasm has not been defined. Therefore, in a randomized, prospective, placebo-controlled study, the authors tested whether prophylaxis with either combined salbutamol-methylprednisolone or salbutamol alone (1) improves lung function and (2) prevents wheezing after intubation. METHODS: Thirty-one patients with partially reversible airway obstruction (airway resistance > 180%, forced expiratory volume in 1 s [FEV1] < 70% of predicted value, and FEV1 increase > 10% after two puffs of salbutamol), who were naive to anti-obstructive treatment, were randomized to receive daily for 5 days either 3 x 2 puffs (0.2 mg) of salbutamol alone (n = 16) or salbutamol combined with methylprednisolone (40 mg/day orally) (n = 15). Lung function was evaluated daily. Another 10 patients received two puffs of salbutamol 10 min before anesthesia. In all patients, wheezing was assessed before and 5 min after tracheal intubation. RESULTS: Within 1 day, both salbutamol and salbutamol-methylprednisolone treatment significantly improved airway resistance (salbutamol, 4.3+/- 2.0 [SD] to 2.9+/-1.3 mmHg x s x l(-1); salbutamol-methylprednisolone, 5.5+/-2.9 to 3.4+/-1.7 mmHg x s x l(-1)) and FEV1 (salbutamol, 1.79+/-0.49 to 2.12+/-0.61 l; salbutamol-methylprednisolone, 1.58+/-0.66 to 2.04+/-1.05 l) to a steady state, with no difference between groups. However, regardless of whether single-dose salbutamol preinduction or prolonged salbutamol treatment was used, most patients (8 of 10 and 7 of 9) experienced wheezing after intubation. In contrast, only one patient receiving additional methylprednisolone experienced wheezing (P = 0.0058). CONCLUSIONS:: Pretreatment with either salbutamol alone or salbutamol combined with methylprednisolone significantly and similarly improves lung function within 1 day. However, only combined salbutamol-methylprednisolone pretreatment decreases the incidence of wheezing after tracheal intubation. Therefore, in patients with bronchial hyperreactivity, preoperative treatment with combined corticosteroids and salbutamol minimizes intubation-evoked bronchoconstriction much more effectively than the inhaled beta2-sympathomimetic salbutamol alone.     

Combined Intravenous Lidocaine and Inhaled Salbutamol Protect against Bronchial Hyperreactivity More Effectively than Lidocaine or Salbutamol Alone

Background: Airway instrumentation in persons with asthma is linked to the risk of life-threatening bronchospasm. To attenuate the response to airway irritation, intravenous lidocaine is recommended (based on animal experiments) and mitigates the response to histamine inhalation in asthmatic volunteers. However, the effects of lidocaine have not been compared with standard prophylaxis with [Greek small letter beta]-sympathomimetic aerosols. Therefore, the effect of lidocaine, salbutamol, combined treatment, and placebo control were tested in awake volunteers with bronchial hyperreactivity.

Methods: After approval from the local ethics committee, 15 persons, who were selected because they showed a decrease in forced expiratory volume in 1 s (FEV1) more than 20% of baseline in response to inhaled histamine in a concentration less than 18 mg/ml (PC20), were enrolled in a placebo-controlled, double-blind, and randomized study. The challenge was repeated on four different days and the volunteers were pretreated with either intravenous lidocaine, inhalation of salbutamol, inhalation of salbutamol plus intravenous lidocaine, or placebo. Lidocaine plasma concentrations were also measured. Statistical analyses included the Friedman test and Wilcoxon's rank sum.

Results: The baseline PC20 was 6.4 +/- 4.3 mg/ml. Intravenous lidocaine and salbutamol aerosol both significantly increased the histamine threshold to 14.2 +/- 9.5 mg/ml and 16.8 +/- 10.9 mg/ml, respectively (mean +/- SD). However, the combination of lidocaine and salbutamol significantly increased the PC20 even further to 30.7 +/- 15.7 mg/ml than did salbutamol or lidocaine alone.     

Lidocaine exerts its effect on induced bronchospasm by mitigating reflexes, rather than by attenuation of smooth muscle contraction

BACKGROUND: Lidocaine inhalation attenuates histamine-induced bronchoconstriction, as well as bronchoconstriction elicited by mechanical irritation. This effect could be mediated by direct effects on smooth muscle or by reflex attenuation. Therefore, we evaluated whether lidocaine attenuated the bronchial response of direct smooth muscle stimulation with methacholine. METHODS: In 15 volunteers with bronchial hyperreactivity, a methacholine challenge was performed following the inhalation of lidocaine, dyclonine (which does not attenuate bronchial reactivity) or saline on three different days in a randomized, double-blind fashion. Lung function, response to methacholine, and lidocaine and dyclonine plasma concentrations were measured. RESULTS: The inhaled methacholine concentration (PC20) necessary for a 20% decrease in the forced expiratory volume in 1 s (FEV1) was 8.8 +/- 6.1 mg/ml at the screening evaluation. The sensitivity to methacholine challenge (PC20) remained unchanged regardless of which solution was inhaled (9.1 +/- 7.5 mg/ml for lidocaine, 10.2 +/- 9.0 mg/ml for dyclonine and 9.8 +/- 8.3 mg/ml for saline; P = 0.58, means +/- standard deviation). Furthermore, the inhalation of all three solutions caused a significant decrease in FEV1 from baseline (P = 0.0007), with a significantly larger effect for dyclonine than lidocaine (P = 0.0153). CONCLUSIONS: Although both inhaled and intravenous lidocaine attenuates histamine-evoked bronchoconstriction, it does not alter the response to methacholine. Therefore, the attenuation of bronchial reactivity by lidocaine appears to be related solely to neurally mediated reflex attenuation, rather than to the attenuation of direct constriction of airway smooth muscle.     

利多卡因对气管平滑肌舒张作用的研究

利多卡因是临床上常用的局部麻醉药和抗室性心律失常药物;除此之外,利多卡因还具有较强的扩张气道、抑制气道炎症、降低气道高反应性的作用。此方面的研究最早可追溯到上世纪60年代,利多卡因在围术期预防和处理支气管痉挛中所占的地位已得到充分肯定,现将近10余年来利多卡因对气道平滑肌影响的主要研究成果综述如下。     

Corticosteroids and Inhaled Salbutamol in Patients with Reversible Airway Obstruction Markedly Decrease the Incidence of Bronchospasm after Tracheal Intubation

Background: In patients with bronchial hyperreactivity, airway instrumentation can evoke life-threatening bronchospasm. However, the best strategy for the prevention of bronchospasm has not been defined. Therefore, in a randomized, prospective, placebo-controlled study, the authors tested whether prophylaxis with either combined salbutamol-methylprednisolone or salbutamol alone (1) improves lung function and (2) prevents wheezing after intubation.

Methods: Thirty-one patients with partially reversible airway obstruction (airway resistance > 180%, forced expiratory volume in 1 s [FEV1] < 70% of predicted value, and FEV1 increase > 10% after two puffs of salbutamol), who were naive to anti-obstructive treatment, were randomized to receive daily for 5 days either 3 x 2 puffs (0.2 mg) of salbutamol alone (n = 16) or salbutamol combined with methylprednisolone (40 mg/day orally) (n = 15). Lung function was evaluated daily. Another 10 patients received two puffs of salbutamol 10 min before anesthesia. In all patients, wheezing was assessed before and 5 min after tracheal intubation.

Results: Within 1 day, both salbutamol and salbutamol-methylprednisolone treatment significantly improved airway resistance (salbutamol, 4.3 +/- 2.0 [SD] to 2.9 +/- 1.3 mmHg [middle dot] s [middle dot] l-1; salbutamol-methylprednisolone, 5.5 +/- 2.9 to 3.4 +/- 1.7 mmHg [middle dot] s [middle dot] l-1) and FEV1 (salbutamol, 1.79 +/- 0.49 to 2.12 +/- 0.61 l; salbutamol-methylprednisolone, 1.58 +/- 0.66 to 2.04 +/- 1.05 l) to a steady state, with no difference between groups. However, regardless of whether single-dose salbutamol preinduction or prolonged salbutamol treatment was used, most patients (8 of 10 and 7 of 9) experienced wheezing after intubation. In contrast, only one patient receiving additional methylprednisolone experienced wheezing (P = 0.0058).     

Cardiovascular responses and lidocaine absorption in fiberoptic-assisted awake intubation

Local anesthetic toxicity and cardiovascular stress during fiberoptic-assisted awake tracheal intubation were assessed prospectively in 20 patients with airway management problems. Cardiovascular responses, dose of lidocaine, its systemic absorption, and patient comfort were measured. A standardized topical anesthesia protocol of 4% lidocaine aerosol, topical 2% lidocaine viscous gel, and direct perbronchoscopic laryngeal application was used. Awake intubation produced no significant elevation of blood pressure or pulse rate either during the topical application or after the intubation. Despite a large total dose of topical lidocaine (5.3 +/- 2.1 mg/kg), the mean peak arterial plasma lidocaine concentration was low (0.6 +/- 2.1 micrograms/ml). Patient comfort assessment showed that nine patients had no discomfort, whereas 11 had minimal discomfort. Supplementary sedation used was minimal (fentanyl, 1.4 +/- 0.6 micrograms/kg, and diazepam, 1.9 +/- 1.8 mg). This method of producing topical anesthesia for awake tracheal intubation is recommended as a safe, easy, and comfortable method of managing patients with airway difficulties.     

The efficacy and safety of EMLA cream for awake fiberoptic endotracheal intubation

EMLA Cream (EC; Astra, Westborough, MA) has been widely used as a local anesthetic. Limited safety information is available with respect to the application of EC to the oral mucous membranes. The purpose of this pilot study was to evaluate the efficacy and safety of EC when applied to oral mucosa for fiberoptic intubation. Twenty ASA physical status I-IV patients (11 women and 9 men), 28-57 yr old, who were scheduled for awake, fiberoptic, intubation participated in this open-label study. A total of 4 g of EC was used for 5 min until the patient showed no evidence of a gag reflex (this was evaluated clinically by the patient's acceptance of the William's airway and considered the endpoint for assessing adequate topicalization of the oropharynx). The measured peak plasma concentration of lidocaine or prilocaine did not reach toxic levels in any patient. Methemoglobin levels did not exceed normal values (1.5%) in any patient, and there was no relationship between methemoglobin levels and patient weight, amount of EC used, measured peak plasma concentration, or times to measured peak concentrations of prilocaine or lidocaine. We conclude that EC provided satisfactory topical anesthesia allowing for successful oral fiberoptic intubation in all patients and should be considered a safe alternative for anesthetizing the airway of patients requiring awake oral fiberoptic intubation.     

Rapid oral anesthesia for awake intubation.

STUDY OBJECTIVE: To determine whether sodium benzonatate (Tessalon Perles) can provide rapid, effective topical oral anesthesia in preparation for awake intubations. DESIGN: Randomized, controlled, single-blind study. SETTING: Medical center anesthesia department. PATIENTS: Forty patients counseled for an awake intubation. INTERVENTIONS: The patients were randomized (random permutated block) to receive either benzonatate 200 mg topically for oropharyngeal anesthesia or bilateral superior laryngeal nerve blocks (total 8 ml of 1% lidocaine) in conjunction with 2 ml of 20% benzocaine orally. Both groups were administered 4 ml of 4% lidocaine translaryngeally. If nasal intubation was anticipated, the patients received 6 ml of 2% lidocaine jelly for nasal anesthesia. MEASUREMENTS AND MAIN RESULTS: The time to obtain oropharyngeal anesthesia was measured as the time from obtaining the benzonatate capsules from the bottle or palpation of the neck to locate the hyoid bone to the time when the patient exhibited an absent gag response to an oropharyngeal airway. After completion of airway preparation, the patient's response to intubation was evaluated by an anesthesiologist blinded to the method of preparation. Medications administered for sedation and analgesia were recorded. Noninvasive blood pressure, heart rate (HR), cardiac rhythm, and three-lead ST segments (I, II, V5) were recorded and evaluated for changes from baseline. Postoperatively, the patient was questioned for recall of the intubation. The time required to obtain loss of the gag response was shorter in the benzonatate group (55.1 +/- 5.7 seconds vs 339 +/- 22.4 seconds, p less than 0.005). The patient response to intubation was similar in both groups (90% no response, 10% minimal response). No abnormal cardiac rhythms or ST segment depression occurred, and mean arterial pressure and HR did not increase more than 20%. CONCLUSIONS: The results of this study indicate that benzonatate capsules provide rapid and reliable oropharyngeal anesthesia in preparation for awake intubation. In addition, if excellent airway anesthesia is provided, awake intubations can be accomplished with minimal patient response and discomfort.     

雾化吸入利多卡因用于颈髓损伤患者纤维支气管镜引导气管插管时表面麻醉的效果

目的 评价雾化吸入利多卡因用于颈髓损伤高位截瘫患者纤维支气管镜(FOB)引导气管插管时表面麻醉的效果.方法 颈椎骨折并发高位截瘫患者64例,随机分为2组(n=32),雾化吸入组:雾化吸入2%利多卡因;喷雾联合环甲膜穿刺组:咽喉部喷雾联合环甲膜穿刺注射2%利多卡因,随后于FOB引导气管插管前15 min,两组均静脉注射咪达唑仑0.01 mg/kg、芬太尼1 μg/kg.FOB引导气管插管期间,评价气管插管条件,监测MAP、HR、ECG及SpO2.结果 与喷雾联合环甲膜穿刺组相比,雾化吸入组气管插管条件满意率和FOB引导气管插管成功率明显提高,心律失常及不良记忆发生率明显降低(P＜0.05).结论 颈髓损伤高位截瘫患者雾化吸入2%利多卡因表面麻醉,有助于改善FOB引导气管插管的条件,且降低不良反应的发生.     

Lidocaine inhalation for local anaesthesia and attenuation of bronchial hyper-reactivity with least airway irritation. Effect of three different dose regimens

The inhalation of lidocaine attenuates bronchial hyper-reactivity but also causes airway irritation. However, how lidocaine dose and plasma concentration influence relationships are unknown. Accordingly, we evaluated the effects of three concentrations of lidocaine (1, 4, and 10%, total dose of 0.5, 2.0, and 5.0 mg kg-1, respectively) vs. placebo in 15 mild asthmatic patients, selected by their response to a histamine challenge (decrease in FEV1 > 20% to less than 18 mg mL-1 of histamine [PC20]). Baseline lung function, histamine-induced bronchoconstriction, topical anaesthesia, and lidocaine plasma concentrations were obtained. FEV1 following lidocaine inhalation showed the greatest decrease for the highest dose (from 3.79 +/- 0.15-3.60 +/- 0.15; P = 0.0012). Lidocaine inhalation increased baseline PC20 (6.1 +/- 1.3 mg mL-1) significantly (to 11.8 +/- 3.1, 16.1 +/- 3.3, and 18.3 +/- 4.5 mg mL-1, respectively) with no difference between the two highest doses. The duration of local anaesthesia was not significantly different between lidocaine concentrations of 4% and 10%. Thus, lidocaine inhalation, with increasing concentrations of the aerosolized solution, increases initial bronchoconstriction while significant attenuation of bronchial hyper-reactivity is not further enhanced with increasing concentrations from 4 to 10%. Plasma concentrations of lidocaine were always far below the toxic threshold. In conclusion, when local anaesthesia of the airways is required a lidocaine dose of 2.0 mg kg-1 as a 4% solution can be recommended for local anaesthesia and attenuation of bronchial hyper-reactivity with the least airway irritation.     

Dexmedetomidine infusion for sedation during fiberoptic intubation: a report of three cases

We report three patients undergoing cervical spine surgery who required awake fiberoptic intubation, and in whom sedation was provided using a dexmedetomidine infusion. Dexmedetomidine was used to provide a moderate level of sedation without causing respiratory distress or hemodynamic instability during fiberoptic intubation. Conditions for intubation were acceptable in all three patients after co-administration of topical anesthesia. Dexmedetomidine may serve as a useful adjunct for this procedure. The anesthetic management and anesthetic implications of using dexmedetomidine infusions for awake fiberoptic intubation are discussed.     

Lung Function under High Thoracic Segmental Epidural Anesthesia with Ropivacaine or Bupivacaine in Patients with Severe Obstructive Pulmonary Disease Undergoing Breast Surgery

Background: Because general anesthesia with tracheal intubation can elicit life-threatening bronchospasm in patients with bronchial hyperreactivity, epidural anesthesia is often preferred. However, segmental high thoracic epidural anesthesia (sTEA) causes pulmonary sympathetic and respiratory motor blockade. Whether it can be safely used for chest wall surgery as a primary anesthetic technique in patients with chronic obstructive pulmonary disease or asthma is unclear. Furthermore, ropivacaine supposedly evokes less motor blockade than bupivacaine and might minimize side effects. To test the feasibility of the technique and the hypotheses that (1) sTEA with ropivacaine or bupivacaine does not change lung function and (2) there is no difference between sTEA with ropivacaine or bupivacaine, the authors studied 20 patients with severe chronic obstructive pulmonary disease (forced expiratory volume in 1 s [FEV1] = 52.1 +/- 17.3% of predicted [mean +/- SD]) or asthma who were undergoing breast surgery.

Methods: In a double-blind, randomized fashion, sTEA was performed with 6.6 +/- 0.5 ml of either ropivacaine, 0.75% (n = 10), or bupivacaine, 0.75% (n = 10). FEV1, vital capacity, FEV1 over vital capacity, spread of analgesia (pin prick), hand and foot skin temperatures, mean arterial pressure, heart rate, and local anesthetic plasma concentrations were measured with patients in the sitting and supine positions before and during sTEA.

Results: Segmental high thoracic epidural anesthesia (segmental spread C4-T8 [bupivacaine] and C5-T9 [ropivacaine]) significantly decreased FEV1 from 1.22 +/- 0.54 l (supine) to 1.09 +/- 0.56 l (ropivacaine) and from 1.23 +/- 0.49 l to 1.12 +/- 0.46 l (bupivacaine). In contrast, FEV1 over vital capacity increased from 64.6 +/- 13.5 to 68.2 +/- 14.5% (ropivacaine) and from 62.8 +/- 12.4 to 66.5 +/- 13.6% (bupivacaine). There was no difference between ropivacaine and bupivacaine. Skin temperatures increased significantly, whereas arterial pressure and heart rate significantly decreased indicating widespread sympathetic blockade. All 20 patients tolerated surgery well.     

Lung function under high thoracic segmental epidural anesthesia with ropivacaine or bupivacaine in patients with severe obstructive pulmonary disease undergoing breast surgery

BACKGROUND: Because general anesthesia with tracheal intubation can elicit life-threatening bronchospasm in patients with bronchial hyperreactivity, epidural anesthesia is often preferred. However, segmental high thoracic epidural anesthesia (sTEA) causes pulmonary sympathetic and respiratory motor blockade. Whether it can be safely used for chest wall surgery as a primary anesthetic technique in patients with chronic obstructive pulmonary disease or asthma is unclear. Furthermore, ropivacaine supposedly evokes less motor blockade than bupivacaine and might minimize side effects. To test the feasibility of the technique and the hypotheses that (1) sTEA with ropivacaine or bupivacaine does not change lung function and (2) there is no difference between sTEA with ropivacaine or bupivacaine, the authors studied 20 patients with severe chronic obstructive pulmonary disease (forced expiratory volume in 1 s [FEV1] = 52.1 +/- 17.3% of predicted [mean +/- SD]) or asthma who were undergoing breast surgery. METHODS: In a double-blind, randomized fashion, sTEA was performed with 6.6 +/- 0.5 ml of either ropivacaine, 0.75% (n = 10), or bupivacaine, 0.75% (n = 10). FEV1, vital capacity, FEV1 over vital capacity, spread of analgesia (pin prick), hand and foot skin temperatures, mean arterial pressure, heart rate, and local anesthetic plasma concentrations were measured with patients in the sitting and supine positions before and during sTEA. RESULTS: Segmental high thoracic epidural anesthesia (segmental spread C4-T8 [bupivacaine] and C5-T9 [ropivacaine]) significantly decreased FEV1 from 1.22 +/- 0.54 l (supine) to 1.09 +/- 0.56 l (ropivacaine) and from 1.23 +/- 0.49 l to 1.12 +/- 0.46 l (bupivacaine). In contrast, FEV1 over vital capacity increased from 64.6 +/- 13.5 to 68.2 +/- 14.5% (ropivacaine) and from 62.8 +/- 12.4 to 66.5 +/- 13.6% (bupivacaine). There was no difference between ropivacaine and bupivacaine. Skin temperatures increased significantly, whereas arterial pressure and heart rate significantly decreased indicating widespread sympathetic blockade. All 20 patients tolerated surgery well. CONCLUSIONS: Despite sympathetic blockade, sTEA does not increase airway obstruction and evokes only a small decrease in FEV1 as a sign of mild respiratory motor blockade with no difference between ropivacaine and bupivacaine. Therefore, sTEA can be used in patients with severe chronic obstructive pulmonary disease and asthma undergoing chest wall surgery as an alternative technique to general anesthesia.     

Intravenous Lidocaine and Bupivacaine Dose-dependently Attenuate Bronchial Hyperreactivity in Awake Volunteers

Background: In standard textbooks, intravenous lidocaine is recommended for intubation of patients with bronchial hyperreactivity. However, whether and to what extent intravenous local anesthetics attenuate bronchial hyperreactivity in humans is unknown. Accordingly, nine awake volunteers with known bronchial hyperreactivity were subjected to an inhalational challenge with acetylcholine before and during intravenous infusion of lidocaine, bupivacaine, or placebo in a randomized, double-blinded fashion.

Methods: Baseline acetylcholine threshold concentrations were determined 3-5 days before initiation of the investigation. The response to the acetylcholine challenge was defined as hyperreactive, if forced expiratory volume in 1 s decreased by at least 20%. In addition, the acetylcholine threshold for a 100% increase in airway resistance was obtained by body plethysmography. On seven different days, the acetylcholine challenge was repeated at the end of a 30-min intravenous infusion period of three doses of lidocaine (1, 3, and 6 mg *symbol* min sup -1) or bupivacaine (0.25, 0.75, and 1.5 mg *symbol* min sup -1), during saline placebo infusion, respectively. Acetylcholine-threshold concentrations were presented with the respective plasma concentrations of the local anesthetic.

Results: The infusion of lidocaine and bupivacaine resulted in plasma concentrations (means+/-SD) of 0.29+/-0.11, 1.14 +/-0.39, and 2.02+/-0.5 micro gram *symbol* ml sup -1 for lidocaine and 0.11+/-0.04, 0.31+/-0.09, and 0.80 +/-0.18 micro gram *symbol* ml sup -1 for bupivacaine, respectively. Compared to baseline, the acetylcholine threshold for a 20% decrease of forced expiratory volume in 1 s as well as the threshold for a 100% increase in total airway resistance increased significantly with increasing plasma concentrations of both local anesthetics. Compared to placebo, acetylcholine threshold was almost quadrupled for lidocaine and tripled for bupivacaine with the highest plasma concentration of each local anesthetic.     

Anesthesia of the airway by aspiration of lidocaine

PURPOSE: Lidocaine instilled onto to the back of the tongue of a supine subject and aspirated has been reported to provide effective topical anesthesia of the airway. The purpose of this study was to observe endoscopically the fate of lidocaine so instilled and document the efficacy of anesthesia for awake fibreoptic intubation. METHODS: In Part I of the study, a fibreoptic bronchoscope was positioned in the pharynx of three volunteers lying supine and the route followed by tinted lidocaine solution instilled onto the back of the protruded tongue during mouth breathing was observed. In Part 2, the airway of 39 patients requiring awake fibreoptic intubation was anesthetized by having them gargle twice with 5 ml lidocaine 2%, followed by instillation of 0.2 ml-kg(-1) or 20 ml lidocaine 1.5% (whichever was less) onto the dorsum of their tongues as described above. The efficacy of anesthesia was scored by the patient reaction (coughing or gagging) to instrumentation in the pharynx, at the glottis, and in the trachea; to passage of the tracheal tube into the trachea; and to the presence of the tube in the trachea. RESULTS: Lidocaine instilled on to the back of the tongue was swallowed initially but ultimately pooled in the pharynx and was aspirated. In all patients the trachea was intubated without requiring supplemental lidocaine, and all but one patient tolerated the tracheal tube in situ. CONCLUSION: A combination of lidocaine gargles and lidocaine instilled on to the back of the tongue and aspirated provides effective anesthesia of the pharynx, larynx, and trachea for awake fibreoptic intubation.     

Cerebral arterial blood flow velocity during induction of general anesthesia: rapid intravenous induction versus awake intubation.

Changes in middle cerebral arterial flow velocity (MCAV) during rapid intravenous induction and awake intubation using transcranial Doppler sonography were investigated. The study involved 20 patients without disorders of the central nervous or cardiovascular systems who were scheduled for maxillofacial surgery. In the intravenous induction group, anesthesia was induced with sodium thiopental, and orotracheal or nasotracheal intubation was facilitated with succinylcholine chloride or alcuronium chloride. In the awake intubation group, orotracheal or nasotracheal intubation was performed under intravenous sedation with diazepam and topical anesthesia with 4% lidocaine. Arterial blood pressures, heart rate, and MCAV were monitored at specific intervals. During intravenous induction, blood pressures decreased after the administration of thiopental and muscle relaxants and increased during endotracheal intubation. MCAV was remarkably slowed after the administration of thiopental and during mask ventilation. During awake intubation, blood pressures were increased by endotracheal intubation. MCAV was decreased from the administration of diazepam to the transtracheal injection of lidocaine, but returned to the control value from endotracheal spray to endotracheal intubation. These results suggest that smooth awake intubation may be the safest method of induction for patients with cerebrovascular disorders.     

Protective effect of drugs on histamine-induced asthma.

Controlled standardised histamine inhalation tests were carried out in 21 asthmatics to determine the degree of non-specific bronchial hyperreactivity with and without prior treatment with several anti-asthmatic drugs. A significant protective effect was produced by inhaled salbutamol, 200 microgram, ingested salbutamol, 4 mg, inhaled Sch1000, 40 microgram inhaled atropine sulphate, 290 microgram, and ingested choline theophylinate (200 or 400 mg) producing serum theophylline levels over 10 mg/l. Inhaled salbutamol was consistently the most effective and was significantly better than the other drugs. The protective effect between the other four was not significantly different. Drug side-effects occurred only with the ingested drugs. No significant protection was detected after ingested choline theophyllinate producing serum theophylline levels of less than 10 mg/l, inhaled sodium cromoglycate, 20 mg given once or six-hourly for one week, or ingested ascorbic acid, 1 gram.