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PubMed1998

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 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. CONCLUSIONS: In volunteers with bronchial hyperreactivity, both lidocaine and salbutamol attenuate the response to an inhalational histamine challenge, and their combined administration has much greater effects than does either drug alone. Accordingly, pretreatment of patients with bronchial hyperreactivity with both beta-mimetic aerosol and intravenous lidocaine is recommended before airway irritation.

Administration, Inhalation↗
PubMed1988

Venous blood concentration of lidocaine after nasopharyngeal application of 2% lidocaine gel.

In 34 subjects undergoing topical anaesthesia with lidocaine gel (2% xylocaine gel), the concentrations of lidocaine base were measured in repeated venous blood samples. Twenty-three patients (Group I) were given 20 ml of 2% lidocaine gel (400 mg of lidocaine) and six subjects (Group II) 40 ml of 2% lidocaine gel (800 mg of lidocaine) nasopharyngeally, the gel reaching the pharynx being swallowed. Five minutes after administration of the gel, a gastric tube was introduced via the nasal cavity. In six patients (Group III), the bladder was catheterised in addition to insertion of a gastric tube. Before the catheter was introduced, these patients were given lidocaine gel nasopharyngeally (400 mg) and endourethrally (400 mg). After the introduction of the gastric tube, all subjects (except four volunteers in Group II) were given general anaesthesia. Before intubation, the patients in Group III also received lidocaine spray laryngotracheally (50 mg; 10% xylocaine spray). The initial absorption of lidocaine was rapid, although the blood concentrations were low. The mean peak concentrations (Cmax) of lidocaine in the three groups were 0.57, 1.39 and 0.73 micrograms/ml, respectively. The blood concentration in Group II was significantly higher than those in Groups I and III. The mean length of time between the nasopharyngeal application of lidocaine gel and the time when Cmax was reached (tpeak) was the same in all three groups (60-70 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMedDate not supplied

A comparison between lidocaine alone and lidocaine with meperidine for continuous spinal anesthesia.

BACKGROUND AND OBJECTIVES: Experimental investigations have demonstrated a synergistic interaction between opioids and local anesthetics. This study aims to assess the effective benefit-risk ratio of continuous spinal anesthesia (CSA) induced with either 1.6% lidocaine alone or in combination with 1% meperidine. METHODS: Thirty-four elderly patients (80.7 +/- 7.3 years) operated on for fracture of the neck of the femur were randomly allocated to two groups. In the first group (n = 15), CSA was induced with lidocaine 1.6% plain, whereas in the second group (n = 19) 1% meperidine was added. Reinjections were performed in both groups using lidocaine 1.6% alone. RESULTS: In the lidocaine group, 43 +/- 13 mg was used for induction whereas in the other group the addition of 18 +/- 5 mg of meperidine significantly reduced the dose of lidocaine required to 28 +/- 8 mg (p < 0.001). Delay between two reinjections was increased to 51 +/- 7 minutes in the lidocaine plus meperidine group, compared to 35 +/- 6 minutes in the lidocaine group (p < 0.001). Ephedrine was required for 9 out of the 19 patients in the lidocaine plus meperidine group, whereas it was required for only two patients in the other group (p = 0.05). Mean plasma concentrations of meperidine 1 hour and 3 hours after induction was 45.5 +/- 12 ng/ml and 59 +/- 22 ng/ml, respectively, and drowsiness was observed in 95% of the patients in the second group. Delay before requirement for pain medication was 2.2 +/- 2 hours in the lidocaine group and 14.1 +/- 8 hours in the lidocaine plus meperidine group (p < 0.001). CONCLUSIONS: The association of 1% meperidine with 1.6% lidocaine during the induction of CSA decreases the initial induction dose, prolongs analgesia, produces initial drowsiness, and provides long-lasting pain relief. However, such benefits are offset by some impairment of hemodynamic stability that is likely to make this combination of drugs unacceptable as an enhanced analgesic technique.

Aged↗
PubMed1977

Effect of lidocaine and methyl lidocaine on cardiac conduction.

The effects of lidocaine and methyl lidocaine on cardiac conduction were studied using His bundle recordings from isolated blood perfused dog hearts. The input and output characteristic of the atrioventricular (AV) node can be described as consisting of three components, namely, minimal conduction time, fatigue, and the effect of prematurity (deltaCT). Lidocaine (2.5-10.0 mg/kg) increased minimal conduction time but not fatigue. Methyl lidocaine (1.25-5.0 mg/kg) increased both. A dose of 5 mg/kg or less of either drug caused a nonparallel shift of the deltaCT curve to the right. High doses of lidocaine (10 mg/kg) cause deltaCT to become rate-dependent. Lidocaine slowed atrial conduction only slightly. Atrial block prevented the observation of the effect of methyl lidocaine in doses higher than 5.0 mg/kg. Both drugs showed greater effect on atrial conduction at fast heart rate. Lidocaine did not affect ventricular conduction time at slow heart rates and had only minimal effects at fast heart rates. Methyl lidocaine increased ventricular conduction time at all heart rates. The results of this study indicate that lidocaine and methyl lidocaine have entirely different spectra of activity on cardiac conduction, in that their effect on AV nodal conduction do not differ greatly whereas the quaternary analog has a much stronger depressant effect on atrial and ventricular conduction.

Animals↗
PubMed1997

Prostaglandin E1, lidocaine, and prostaglandin E1-lidocaine combination for attenuating cardiovascular responses to extubation.

PURPOSE: Tracheal extubation produces haemodynamic changes that may cause myocardial ischaemia in patients with coronary arterial disease. Intravenous infusion of prostaglandin E1 (PGE1) attenuated the hypertensive response to tracheal extubation but failed to blunt the tachycardia, which was attenuated by intravenous lidocaine. Thus, we investigated whether a combination of PGE1 and lidocaine can overcome the drawbacks of treatment with PGE1 alone. METHODS: One hundred adult patients (ASA 1) undergoing elective minor surgery were randomly assigned to receive one of four treatments: saline (as a control), 1 mg-kg-1 lidocaine, infusion of 0.1 microgram-1.kg-1.min-1 PGE1, or infusion of 0.1 microgram-1.kg-1.min-1 PGE1 plus injection of 1 mg-1.kg-1 lidocaine. Lidocaine was injected two minutes before tracheal extubation. The PGE1 was infused from completion of surgery until five minutes after tracheal extubation. Anaesthesia was maintained with sevoflurane 1.0%-2.5% and nitrous oxide 60%. Heart rate (HR) and blood pressure (BP) were measured before and after tracheal extubation. RESULTS: Lidocaine alone and PGE1-lidocaine combination attenuated the increases in BP and HR observed in the control group: PGE1 alone was effective in attenuating hypertensive response but ineffective for tachycardia. The suppressive effect of the PGE1-lidocaine combination on BP increase was superior to that of each drug alone, and the combined effect on HR increase was similar to that of lidocaine alone. CONCLUSION: The combination of PGE1 infusion and lidocaine is a more effective method of attenuating hypertension and tachycardia associated with tracheal extubation than either drug alone.

Adult↗
PubMed1999

Growth of Escherichia coli in propofol, lidocaine, and mixtures of propofol and lidocaine.

BACKGROUND: Microorganisms grow rapidly in propofol. Extrinsic contamination of propofol is thought to be a source of postoperative sepsis and wound infection. We studied growth of a strain of Escherichia coli in thiopental, propofol, lidocaine, and mixtures of propofol and lidocaine. METHODS: The pathogen was exposed to 2.5% thiopental; 1.0% propofol; 1.0%, 2.0% and 4.0% preservative-free lidocaine; and propofol solutions containing 0.25%, 0.5%, 1.0%, 2.0%, or 4.0% lidocaine for 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, and 24 h at room temperature, respectively. The inocula from these suspensions were cultured for 48 h at 37 degrees C after the antimicrobial activity of the local anesthetics in the inocula was inactivated by a 1:1000 dilution with distilled water. RESULTS: No organisms grew after exposure to 2.5% thiopental. The exposure of E. coli to propofol increased the colony count to approximately 90 times the control count. The colony counts of E. coli after exposure to 1.0%, 2.0% and 4.0% lidocaine and 0.25%, 0.5%, 1.0%, 2.0% and 4.0% lidocaine in 1.0% propofol were lower than the counts after exposure to 1.0% propofol (P = 0.0048, 0.0027, 0.0003, 0.0503, 0.0188, 0.0080, 0.0044, and 0.0001, respectively). The growth rate of the microorganism was significantly higher in cultures exposed to 1.0% propofol than that in cultures exposed to lidocaine alone or lidocaine-propofol mixtures (P < 0.0001, respectively). CONCLUSION: Lidocaine possesses bacteriostatic activity against E. coli. Addition of lidocaine to propofol confers its bacteriostatic activity to the mixture and may decrease the hazard of infection associated with the extrinsic contamination of propofol.

Anesthetics, Intravenous↗
PubMedDate not supplied

Postoperative analgesia after peripheral nerve block for podiatric surgery: clinical efficacy and chemical stability of lidocaine alone versus lidocaine plus ketorolac.

BACKGROUND AND OBJECTIVES: The purpose of this study was to determine whether the addition of ketorolac tromethamine to local anesthesia for ankle block alters the quality or duration of analgesia after podiatric surgery. The second aim was to determine the chemical stability of ketorolac tromethamine when added to local anesthetic solutions. METHODS: The study design was double-blinded, placebo-controlled, and randomized. Seventy-nine American Society of Anesthesiologists (ASA) class I or II patients scheduled for bunionectomy or hammer toe repair, or both were randomized to 1 of 4 groups. Group L received plain 1.73% lidocaine for their ankle block. Group K received 1.73% lidocaine with ketorolac (4 mg/mL) added to the local solution. Group Kiv received 1.73% plain lidocaine for ankle block and 20 mg of ketorolac intravenously. Group E received 1.73% lidocaine with .67% ethanol added. The final concentration of lidocaine for all groups was 1.73%. The block performed in each patient was a 5-point ankle block. Beginning at 1 hour after the completion of the block and every 30 minutes thereafter, visual analogue scale (VAS) and verbal pain scores were recorded. The time from performance of the block to the initial pain and time to the first oral pain medication intake were also recorded. The time and amount of postoperative oral analgesics in the first 9 hours after the block were recorded. Adverse events were also recorded for each group. RESULTS: There were significantly lower overall VAS and verbal pain scores for group K compared with groups E and L and group Kiv compared with group E. Group K also had a significantly longer time to the first reported pain and first oral pain medications than groups E and L, but not with Group Kiv. The same group had significantly fewer average doses of pain medications postoperatively than Groups E and L. Group E had significantly shorter times to first report of pain and first pain medications and higher mean dose of postoperative oral analgesics than group K and Group Kiv. There were no untoward side effects reported from any group. Chemical analysis by gas chromatography (GC) and capillary electrophoresis (CE) showed no significant change in composition of the solutions when ketorolac was mixed with lidocaine and/or bupivacaine and stored at 37 degrees C for 1 week. CONCLUSIONS: The addition of ketorolac to lidocaine for ankle block contributed to longer duration and better quality analgesia after foot surgery compared with plain 1.73% lidocaine or 1.73% lidocaine plus intravenous ketorolac. The ethanol vehicle is unlikely responsible for the analgesic effects of ketorolac. Ketorolac retains its chemical stability when placed in local solutions of lidocaine or bupivacaine.

Adult↗
PubMed2000

A comparison of minidose lidocaine-fentanyl and conventional-dose lidocaine spinal anesthesia.

The syndrome of transient neurologic symptoms (TNS) after spinal lidocaine has been presumed to be a manifestation of local anesthetic neurotoxicity. Although TNS is not associated with either lidocaine concentration or dose, its incidence has never been examined with very small doses of spinal lidocaine. One hundred ten adult ASA physical status I and II patients presenting for arthroscopic surgery of the knee were randomly assigned to receive spinal anesthesia with either 1% hypobaric lidocaine 50 mg (Group L50) or 1% hypobaric lidocaine 20 mg + 25 microg fentanyl (Group L20/F25). Hemodynamic data, block height and regression, and time to first micturition and discharge were recorded. Follow-up phone calls were made by a blinded researcher at 48-72 h using a standardized questionnaire. Both groups had a median peak cephalad block level of T10. Lidocaine 50 mg was associated with a greater decrease in systolic blood pressure and a greater need for ephedrine. Time until block regression to the S2 dermatome (80 vs. 110 min) and outpatient time to void (130 vs 162 min) and discharge (145 vs. 180 min) were faster in the L20/F25 group. Complaints of TNS were found in 32.7% of the patients in the L50 group and in 3.6% of the patients in the L20/F25 group. We conclude that spinal anesthesia with lidocaine 20 mg + fentanyl 25 microg provided adequate anesthesia with greater hemodynamic stability and faster recovery than spinal anesthesia with lidocaine 50 mg. The incidence of TNS after spinal lidocaine 20 mg + fentanyl 25 microg was significantly less than that after spinal lidocaine 50 mg.

Adjuvants, Anesthesia↗
PubMed2004

Identification of the epidural space: loss of resistance with air, lidocaine, or the combination of air and lidocaine.

The ideal technique for identifying the epidural space remains unclear. Five-hundred-forty-seven women in labor who requested epidural analgesia were randomly allocated to three groups according to the technique by which the epidural space was identified: 1) loss-of-resistance with air (air; n = 180), 2) loss-of-resistance with lidocaine (lidocaine; n = 185), and 3) loss-of-resistance with both air and lidocaine (air-plus-lidocaine; n = 182). We assessed ease of epidural catheter insertion, characteristics of the blockade, quality of analgesia, and complications. The inability to thread the epidural catheter occurred in 16% of the air, 4% of the lidocaine, and 3% of the air-plus-lidocaine patients (P < 0.001). More patients from the air group had unblocked segments (6.6% versus 3.2% and 2.2%, respectively; P < 0.02). The incidence of accidental dural puncture was greater in the air group (1.7% versus 0% in the other two groups; P < 0.02). Pain scores, time to onset of analgesia, upper sensory level, motor blockade, and the incidence of hypotension, transient neurological deficits, postpartum urinary retention, and postdural puncture headache were comparable. Identification of the epidural space with air was more difficult and caused more dural punctures than with lidocaine or air plus lidocaine. Additionally, sequential use of air and lidocaine had no advantage over lidocaine alone.

Adolescent↗
PubMedDate not supplied

Lidocaine hydrocarbonate is not superior to lidocaine hydrochloride in interscalene brachial plexus block.

To determine the effect of carbonation of lidocaine, a comparison of 1.0% lidocaine hydrochloride (HCl) and 1.1% lidocaine hydrocarbonate (CO2), both with 1:200,000 epinephrine, was made in this study of 50 patients receiving interscalene brachial plexus blocks. Sensory block was determined by the response to pinprick in the C2-T2 dermatomes, while motor block was assessed by the development of paresis and paralysis at the shoulder and hand. The percentage of patients developing analgesia (decreased sensation to pinprick) and anesthesia (total absence of sensation to pinprick) at each dermatome level as well as the percentage of patients developing motor block was not significantly different between the two forms of lidocaine. The initial onset of analgesia [lidocaine HCl, 4.0 +/- 2.4 (SD) minutes; lidocaine CO2, 4.3 +/- 3.8 (SD) minutes] and anesthesia [lidocaine HCl, 10.1 +/- 5.7 (SD) minutes; lidocaine CO2, 7.8 +/- 4.4 (SD) minutes] did not differ significantly between the two groups. At the individual dermatomes, there was no difference in the onset of analgesia except at one dermatome level, C7, which was near the level of local anesthetic injection. Anesthesia onset in each dermatome as well as the onset of motor block did not differ between the two groups. It is concluded that lidocaine CO2 does not offer any significant clinical advantage over lidocaine HCl in interscalene brachial plexus block.

Adult↗
PubMed1994

Comparison of absorption of aqueous lidocaine and liposome lidocaine following topical application on rabbit vessels.

Liposomes are small particles that encapsulate lidocaine to form topical drug carriers. Forty rabbits were used to compare the absorption of aqueous lidocaine with that of liposome lidocaine after application of each on femoral and iliac vessels. Both agents entered the circulation rapidly. The serum levels of lidocaine were significantly lower and the peaks in concentration appeared later after the use of liposome lidocaine than after the use of aqueous lidocaine. This phenomenon was due to local accumulation of liposome lidocaine and slow release of lidocaine from the liposome. As a topical spasmolytic agent, liposome lidocaine may be superior to the aqueous form due to a lower serum concentration and less total absorption.

Absorption↗
PubMedDate not supplied

Effects of AN-132, a novel antiarrhythmic lidocaine analogue, and of lidocaine on membrane ionic currents of guinea-pig ventricular myocytes.

We studied the effects of AN-132 (10, 30 and 100 mumol/l), an analogue of lidocaine, on membrane currents and action potentials of single guinea-pig ventricular cells using whole-cell clamp techniques. The effects of lidocaine, an authentic class I antiarrhythmic agent were used for comparative purposes. (1) AN-132 decreased the Na current (INa) in a concentration-dependent manner, with a greater efficacy than seen with lidocaine. The concentration of the half maximal inhibition on INa (Kd) was 31.7 mumol/l for AN-132 and 94.9 mumol/l for lidocaine. (2) AN-132 also decreased the Ca current (ICa), concentration-dependently, while lidocaine had only a minor effect on ICa. The half maximal inhibition on ICa (Kd) was 23.1 mumol/l and 27.4 mumol/l for AN-132 and lidocaine, respectively. (3) AN-132 decreased the IK1, in a concentration-dependent manner; lidocaine was without effect. (4) AN-132 increased the unspecified steady state outward current, at positive potentials and depressed the time- and voltage-dependent outward K current (IK). Lidocaine had no effect on either current. (5) AN-132 shortened the action potential duration (APD), in a concentration-dependent manner, without altering the resting potential. From these findings, we conclude that apart from a potent inhibitory effect on INa, AN-132 had a variety of effects on other currents, properties not shared by lidocaine. Such multiple blocking effects on the membrane currents may relate to the alleged potent antiarrhythmic effect of AN-132.

Anilides↗
PubMed1995

Does topical lidocaine attenuate the pain of infiltration of buffered lidocaine?

OBJECTIVE: To determine whether topical lidocaine attenuates the pain of buffered lidocaine infiltration. METHODS: This was a prospective, randomized, double-blind, placebo-controlled trial conducted at a university-based ED. The subjects were adults who had lacerations being repaired using local anesthesia. Two 0.5-mL injections of buffered lidocaine were given in a standardized manner. The first was given prior to application of topical study solution. The second was given on the opposite side of the laceration after topical application of study solution, which was 5 mL of either 2% lidocaine or saline placebo. The pain of each infiltration was measured using a visual analog pain scale. Pain scores were calculated and compared using a Wilcoxon test with significance defined as p < or = 0.05. RESULTS: A total of 54 subjects participated; 29 received lidocaine topically and 25 received placebo. The groups were similar with respect to age, gender, wound length, wound location, and initial pain score. Pain scores decreased by 11.6 +/- 18.6 mm for lidocaine and 10.9 +/- 20.9 mm for placebo (p > 0.5). The study had the power to detect a 15-mm pain score difference (alpha = 0.05 and beta = 0.20) on a 100-mm scale. CONCLUSION: Topical 2% lidocaine does not attenuate the pain of infiltration of buffered lidocaine more than does topical normal saline. Investigation of other topical anesthetics with and without epinephrine in conjunction with buffered lidocaine is warranted.

Administration, Cutaneous↗
PubMed1990

Electrophysiological effects of the clinically used local anesthetics lidocaine, lidocaine-prilocaine and phenol on the rat's inner ear.

Local anesthetics, even if applied to the outer ear canal, may still enter the middle ear, running the risk of penetrating the round window. To elucidate the effect of certain topical anesthetics on the inner ear, the round window niche in the laboratory rat's middle ear was exposed separately to lidocaine, lidocaine-prilocaine and phenol. Auditory brain-stem responses (ABR) were recorded at 2, 4, 6, 8, 12, 16, 20, and 31.5 kHz before the application, and 24 h, 3 weeks, 2 months and 6 months after exposure. After terminating the 6-month ABR measurements, the animal were sacrificed and the temporal bones fixed and decalcified for light microscopic analysis. All three drugs affected the ABR thresholds and the cochlear morphology with a pattern characteristic for each drug. At 24 h, all three substances caused severe impairment of ABR thresholds, followed by a period of restitution lasting up to 2 months. Even 6 months after exposure, the ABR thresholds at and above 12 kHz were impaired, as compared with the pretreatment level, for all substances tested. In the lower frequencies the original ABR threshold was reached in the order: (1) lidocaine, (2) lidocaine-prilocaine, (3) phenol. The cochlear structures were unaffected by lidocaine, whereas lidocaine-prilocaine and phenol caused morphological damage which was most pronounced after exposure to phenol. The heterogeneity of the changes in the ABR thresholds suggests differences in the mechanism of action of each type of local anesthetic investigated. The effects following lidocaine were transient. However, clinicians must be aware of the ototoxic potential of both lidocaine and phenol.

Anesthetics, Local↗
PubMed1990

Plasma lidocaine concentrations during continuous epidural infusion of lidocaine with and without epinephrine.

Plasma lidocaine concentrations were measured over a five-hour period in 20 patients following continuous epidural infusion of lidocaine for surgical anaesthesia. Patients were divided into two groups: Group I received plain lidocaine; Group II received lidocaine with epinephrine. Patients initially received 10 ml followed by a constant infusion of 10 ml.hr-1 of two per cent lidocaine. The mean plasma concentrations of lidocaine were significantly higher for the first 40 min in Group I than in Group II. However, from one to five hours, there was no significant difference between the groups. These results demonstrate that the addition of epinephrine to lidocaine does not decrease the plasma concentration of lidocaine during continuous epidural infusion for long operations.

Abdomen↗
PubMed1997

Attenuation of cardiovascular responses to tracheal extubation: comparison of verapamil, lidocaine, and verapamil-lidocaine combination.

UNLABELLED: We recently showed that verapamil attenuated hemodynamic responses to tracheal extubation. The aim of the current study was to compare the efficacy of a combination of intravenous (I.V.) verapamil (0.1 mg/kg) and I.V. lidocaine (1 mg/kg) with that of each drug alone in suppressing the cardiovascular changes during tracheal extubation and emergence from anesthesia. One hundred adult patients (ASA physical status I) who were to undergo elective minor surgery were randomly assigned to one of four groups (n = 25 each): Group S = saline plus saline (control), Group V = verapamil 0.1 mg/kg I.V. plus saline, Group L = lidocaine 1 mg/kg I.V. plus saline, and Group V-L = verapamil 0.1 mg/kg I.V. plus lidocaine 1 mg/kg I.V. These medications were given 2 min before tracheal extubation. Anesthesia was maintained with 1.0%-2.0% sevoflurane and 60% nitrous oxide (N2O) in oxygen. Muscle relaxation was achieved with vecuronium, and a residual neuromuscular blockade was reversed with neostigmine 0.05 mg/kg (combined with atropine 0.02 mg/kg). Changes in heart rate (HR) and arterial blood pressure (AP) were measured during and after tracheal extubation. In the control group, the HR and systolic and diastolic AP increased significantly during tracheal extubation. Verapamil, lidocaine, and their combination attenuated the increases in these variables. The beneficial effect was the greatest with the combination of verapamil and lidocaine. These findings suggest that verapamil 0.1 mg/kg and lidocaine 1 mg/kg given I.V. concomitantly 2 min before tracheal extubation is a simple and more effective prophylaxis than verapamil or lidocaine alone for attenuating the cardiovascular changes associated with tracheal extubation. IMPLICATIONS: Tachycardia and hypertension associated with tracheal extubation, which may lead to myocardial ischemia, represent a potential risk for patients with coronary arterial disease. To seek effective pharmacological prophylaxis against these complications, we compared the attenuation of hemodynamic changes among verapamil, lidocaine, and a verapamil/lidocaine combination using ASA physical status I patients and found the combination to be effective.

Adult↗
PubMed1997

A comparative efficacy study of hyperbaric 5% lidocaine and 1.5% lidocaine for spinal anesthesia.

UNLABELLED: We compared the clinical efficacy of 1.5% lidocaine in dextrose 7.5% in water, which is currently available as a commercial preparation but approved for use only in obstetrical patients, with the traditional 5% lidocaine in dextrose 7.5% in water for spinal anesthesia in patients undergoing lower abdominal procedures. Fifty-one male patients scheduled to undergo inguinal herniorrhaphy were randomly divided into two groups based on the spinal anesthetic received: Group I received 1.5% lidocaine in dextrose 7.5% in water, and Group II received 5% lidocaine in dextrose 7.5% in water. After intrathecal injection of the anesthetic, each patient was evaluated for the speed of onset, the time to recovery, and the quality of the surgical anesthesia and motor block that ensued by an anesthesiologist blinded to the technique. With the exception of the patients in Group I, who achieved a higher dermatome level of sensory analgesia, we were unable to demonstrate any significant clinical differences between the two lidocaine solutions. Our results indicate that lidocaine 1.5% in dextrose 7.5% in water is clinically indistinguishable from the 5% solution as a spinal anesthetic for lower abdominal surgery. IMPLICATIONS: In this study, two concentrations of lidocaine are compared as spinal anesthetics in 51 male patients undergoing inguinal hernia repair. Patients were assessed for the onset, quality, and duration of the spinal block. The study results indicate that 1.5% lidocaine is as effective as the 5% solution as a spinal anesthetic for patients undergoing inguinal hernia repair.

Adolescent↗
PubMed1992

Lidocaine hydrocarbonate and lidocaine hydrochloride for cesarean section: transplacental passage and neonatal effects.

Twenty-six patients, ASA physical status 1, scheduled for elective cesarean section, were divided at random into two groups and received via an epidural catheter 20 ml of 2.2% lidocaine hydrocarbonate (17.3 mg.ml-1 lidocaine base) with 5 micrograms.ml-1 epinephrine freshly added (Group CO2 = 13 patients) or 20 ml of 2% lidocaine hydrochloride (17.3 mg.ml-1 lidocaine base) also with 5 micrograms.ml-1 epinephrine freshly added. Following clampage of the umbilical cord (at 40.1 +/- 4.9 min after the injection of lidocaine for the CO2 group and at 41.0 +/- 5.4 min for the HCl group), serum concentrations of lidocaine were measured both in the mother and in the umbilical vein. All newborns were examined by the same blinded pediatrician with Apgar scores at 1, 5 and 10 min and with Neurobehavioral Adaptive Capacity Scores (NACS) at 15 min, 2 h and 24 h. The concentrations of lidocaine in the serum were comparable in both groups: in the mothers 8.61 +/- 1.48 mumol.l-1 for the CO2 group vs 8.04 +/- 2.36 mumol.l-1 for the HCl group and in the newborns 3.86 +/- 0.84 mumol.l-1 for the CO2 group vs 3.92 +/- 0.95 mumol.l-1 for the HCl group. The ratio of umbilical vein to maternal vein concentrations of lidocaine was also similar in both groups: 0.45 +/- 0.07 for the CO2 group vs 0.54 +/- 0.24 for the HCl group. The percentage of newborns with a normal NACS (score > or = 35/40) was equal in both groups, i.e. 91% at 15 min and 2 h of life and 100% at 24 h of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗