Free lidocaine concentrations during continuous epidural anesthesia in geriatric patients

BACKGROUND AND OBJECTIVES: To evaluate the effects of aging on lidocaine pharmacokinetics, the plasma concentrations of total and free lidocaine and its metabolites were measured during continuous thoracic epidural anesthesia in middle-aged (age 41 +/- 9 years, n = 7) and elderly (age 72 +/- 2 years, n = 7) male patients. METHODS: After establishment of general anesthesia, 7 mL 1.5% lidocaine with epinephrine 1:200,000 was injected into the epidural space and subsequently infused at a rate of 5 mL/h for 5 hours. Plasma concentrations of total and free lidocaine, monoethylglycinexylidide (MEGX), and glycinexylidide (GX) were measured at 10, 15, 20, 30, 45, 60, 90, 120, 150, 180, 240, and 300 minutes after initial lidocaine injection using high-performance liquid chromatography (HPLC) with ultraviolet (UV) detection. RESULTS: The elderly group showed a stronger upward trend in the corrected free lidocaine concentrations and lower corrected total MEGX concentrations than the middle-aged group. CONCLUSIONS: Lidocaine metabolite activity in the elderly male patients was lower than that in the middle-aged male patients. Free lidocaine concentration is prone to increase in elderly patients. Caution must be exercised during continuous thoracic epidural anesthesia combined with general anesthesia in geriatric patients.     

Small-dose dopamine increases epidural lidocaine requirements during peripheral vascular surgery in elderly patients

We studied 20 patients over the age of 65 yr undergoing prolonged peripheral vascular surgery under continuous lidocaine epidural anesthesia, anticipating that the increased hepatic metabolism caused by small-dose IV dopamine would lower plasma lidocaine concentrations. Subjects were assigned (random, double-blinded) to receive either a placebo IV infusion or dopamine, 2 microg. kg(-1). min(-1) during and for 5 h after surgery. Five minutes after the IV infusion was started, 20 mL of 2% lidocaine was injected through the epidural catheter. One-half hour later, a continuous epidural infusion of 2% lidocaine at 10 mL/h was begun. The epidural infusion was temporarily decreased to 5 mL/h or 5 mL boluses were added to maintain a T8 analgesic level. Arterial blood samples were analyzed for plasma lidocaine concentrations regularly during and for 5 h after surgery. Plasma lidocaine concentrations increased continuously during the epidural infusion and, despite wide individual variation, were similar for the two groups throughout the observation period. During the observation period, the mean maximal plasma lidocaine concentration was 5.8 +/- 2.3 microg/mL in the control group and 5.7 +/- 1.2 microg/mL in the dopamine group. However, the mean hourly lidocaine requirement during surgery was significantly different, 242 +/- 72 mg/h for control and 312 +/- 60 mg/h for dopamine patients (P < 0.03). At the end of Hour 4, the last period when all 20 patients were still receiving the epidural lidocaine infusion, the total lidocaine requirement was significantly different, 1088 +/- 191 mg for the control group and 1228 +/- 168 mg for the dopamine group (P < 0.05). Despite very large total doses of epidural lidocaine (1650 +/- 740 mg, control patients, and 1940 +/- 400, dopamine patients) mean maximal plasma concentrations remained below 6 microg/mL, and no patient exhibited signs or symptoms of toxicity. We conclude that small-dose IV dopamine increased epidural lidocaine requirements, presumably as a consequence of increased metabolism. IMPLICATIONS: We tested dopamine, a drug that increases liver metabolism of the local anesthetic lidocaine to determine if it would prevent excessively large amounts of lidocaine in the blood during prolonged epidural anesthesia in elderly patients. Dopamine did not alter the blood levels of lidocaine, but it did increase the lidocaine dose requirement to maintain adequate epidural anesthesia.     

Anesthesia for creation of a forearm fistula in patients with endstage renal failure

The effects of local infiltration anesthesia, brachial plexus blockade, isoflurane, or halothane anesthesia on blood flow through the brachial artery and through a newly created forearm arteriovenous fistula (AVF) were compared in 36 patients with endstage renal failure. Brachial artery blood flow was measured at two different times, before anesthesia and during anesthesia but before surgery, using a pulsed Doppler flowmeter. AVF flows were calculated from brachial, radial, and ulnar blood flows at the end of surgery, 2 h after surgery, and 3 and 10 days after the procedure. Mean arterial pressure was lower in patients receiving isoflurane or halothane than in those receiving local anesthesia or brachial plexus blockade (BPB). There was a significant increase in brachial artery blood flow following BPB (43.7 +/- 18.7 to 186.9 +/- 98.2 ml.min-1) during isoflurane anesthesia (46.2 +/- 15.9 to 153.1 +/- 80.5 ml.min-1) and during halothane anesthesia (49.9 +/- 24.1 to 97.6 +/- 62.1 ml.min-1). During anesthesia, the difference in brachial artery blood flow between patients in the BPB and halothane groups was significant. Local anesthesia failed to increase brachial artery blood flow (44.0 +/- 12.7 to 45.6 +/- 11.3 ml.min-1). In the immediate postoperative period, the AVF blood flow was lower in patients in the halothane group than in the other groups, but this difference was only significant when compared with BPB group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Does choice of the anesthetic influence renal function during infrarenal aortic surgery?

Reconstructive infrarenal aortic surgery is associated with impairment of renal function owing to vasoconstriction during and after aortic cross-clamping. To assess the influence of anesthetic technique on renal hemodynamics during aortic surgery, 34 patients received one of four anesthetics: isoflurane (n = 10), halothane (n = 9), droperidol (n = 8), and flunitrazepam (n = 7). Supplemental anesthesia consisted of midazolam, fentanyl, nitrous oxide in oxygen (50%), and pancuronium. Before aortic cross-clamping, effective renal plasma flow (ERPF) (131iodohippuran clearance) and glomerular filtration rate (GFR) (99technetium-DTPA clearance) were low in the halothane and flunitrazepam groups (118.4 +/- 25.6 and 170 +/- 35 mL/min for ERPF; 19.7 +/- 5.2 and 26.9 +/- 5.8 mL/min for GFR, respectively) and better preserved in the isoflurane group (253.4 +/- 51.5 and 44.9 +/- 8.4 mL/min, respectively; P less than 0.05 between isoflurane and halothane groups) or in the droperidol group as regards GFR (75.4 +/- 9.4 mL/min, P less than 0.05). During clamping, both renal variables were not markedly affected in any group except in the droperidol group in whom GFR significantly decreased from preclamp value. The GFR was then significantly higher in the isoflurane group (49.5 +/- 9.2 mL/min) than in the halothane and flunitrazepam groups (14.8 +/- 3.7 and 26.5 +/- 10.1 mL/min, respectively; P less than 0.05). After aortic declamping, ERPF and GFR increased markedly in the halothane group, and there was no significant difference between the groups. These results suggest that renal hemodynamics are less altered with droperidol-fentanyl anesthesia during abdominal surgery but not during aortic cross-clamping.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of epidural insertion site and surgical procedure on plasma lidocaine concentration

We compared the plasma lidocaine concentrations associated with continuous epidural infusion at different insertion sites in patients during surgery using epidural plus general anesthesia. In Study 1, there were 12 patients in each of four surgical groups in whom blood loss was expected to be <400 mL. The four groups were as follows: the lower extremity, the lower abdomen, the upper abdomen, and the lung. Liver surgery was excluded from Study 1. Study 2 comprised patients undergoing radical hysterectomy or radical prostatectomy (a radical operation group, n = 12) and hepatectomy (a hepatectomy group, n = 12) in whom the expected surgical blood loss was more than 1500 mL. All patients initially received 0.1 mL/kg followed by a continuous infusion of 0.1 mL. kg(-1). h(-1) of 1.5% lidocaine, and plasma concentrations of lidocaine were measured at 15, 30, 60, 90, and 120 min and every 60 min thereafter to 300 min. The plasma lidocaine concentration during surgery did not change regardless of the infusion site or the surgical site, other than the liver. The plasma concentrations of lidocaine in the hepatectomy group increased significantly at 180 min (2.9 +/- 0.6 microg/mL, P < 0.01), 240 min (3.5 +/- 0.7 microg/mL, P < 0.01), and 300 min (3.6 +/- 0.74 microg/mL, P < 0.01) compared with that at 15 min (2.0 +/- 0.3 microg/mL), and these values were significantly larger than those in all other groups.     

Comparative hemodynamic depression of halothane versus isoflurane in neonates and infants: an echocardiographic study.

The purpose of this study was to measure and compare the relationship of cardiovascular depression and dose during equal potent levels of halothane and isoflurane anesthesia in neonates (n = 19) (16.7 +/- 6.9 days) and infants (n = 54) (6.1 +/- 3.1 mo). Seventy-three children had heart rate, arterial blood pressure, and pulsed Doppler pulmonary blood flow velocity as well as two-dimensional echocardiographic assessments of left ventricular area and length recorded just before anesthesia induction. Anesthesia was induced by inhalation of increasing inspired concentrations of halothane or isoflurane in oxygen using a pediatric circle system and mask. During controlled ventilation, halothane and isoflurane concentrations were adjusted to maintain 1.0 MAC and then 1.5 MAC (corrected for age), and echocardiographic and hemodynamic measurements were repeated. A final cardiovascular measurement was recorded after intravenous administration of 0.02 mg/kg of atropine. All measurements were completed before tracheal intubation and the start of elective surgery. In neonates, 1.0 MAC concentrations of halothane and isoflurane decreased cardiac output (74% +/- 16%), stroke volume (75% +/- 15%), and ejection fraction (76% +/- 15%) similarly from awake levels. Decreases in cardiac output, stroke volume, and ejection fraction with halothane and isoflurane were significantly larger at 1.5 MAC (approximately 35% decreases from awake values) than at 1.0 MAC. Heart rate decreased significantly during 1.5 MAC halothane anesthesia (94% +/- 4%) but remained unchanged during isoflurane anesthesia. In infants, 1.0 MAC halothane and isoflurane decreased cardiac output (83% +/- 12%), stroke volume (78% +/- 12%), and ejection fraction (74% +/- 12%) when compared with awake measures.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of halothane and isoflurane on transient renal dysfunction associated with infrarenal aortic cross-clamping.

Aortic cross-clamping for reconstructive aortic surgery is associated with impairment of renal function. Halothane or isoflurane was used to assess the influence of volatile anesthesia on renal hemodynamics during aortic surgery. Nineteen patients with normal preoperative creatinine clearances who were scheduled for reconstructive aortic surgery were randomly divided into two groups: halothane group (n = 9) and isoflurane group (n = 10). Induction of anesthesia consisted of midazolam, fentanyl, and pancuronium. Anesthesia was maintained with fentanyl and halothane or isoflurane in nitrous oxide and oxygen (50/50). Systemic hemodynamics were similar in both groups throughout surgery. Before aortic cross-clamping, effective renal plasma flow (ERPF) (131I-hippuran clearance) and glomerular filtration rate (GFR) (99Tc-DTPA clearance) were significantly lower in the halothane group (118.4 +/- 25.6 and 19.7 +/- 5.2 mL/min, respectively) than in the isoflurane group (253.4 +/- 51.5 and 44.9 +/- 8.4 mL/min) (P less than 0.05 for both). During cross-clamping, the renal variables were not markedly affected in either group and remained higher in the isoflurane-anesthetized patients (232.9 +/- 47.1 and 49.5 +/- 1.2 mL/min for ERPF and GFR, respectively) than in the halothane-anesthetized patients (132.4 +/- 31.6 and 14.8 +/- 3.7 mL/min, respectively) (P less than 0.05). After aortic unclamping, ERPF increased markedly in both groups (467.8 +/- 122 and 362.5 +/- 57.7 mL/min in the halothane and isoflurane groups, respectively), as did GFR (74.8 +/- 22 and 71.8 +/- 13.1 mL/min, respectively). These results suggest that anesthesia with halothane is associated with transient renal vasoconstriction during abdominal surgery. In contrast, aortic cross-clamping during isoflurane anesthesia was not associated with renal hemodynamic impairment.     

Reversal of lidocaine with epinephrine epidural anesthesia using epidural saline washout

BACKGROUND AND OBJECTIVES: Prolonged motor and sensory block following epidural anesthesia can be associated with extended postoperative care unit stays and patient dissatisfaction. Previous studies have demonstrated a more rapid motor recovery following the administration of epidural crystalloids in patients who had received plain bupivacaine and lidocaine epidural anesthesia. However, epinephrine is commonly added to local anesthetics to improve the quality and prolong the duration of the epidural block. The objective of this study was to determine the relationship of 0.9% NaCl epidural catheter flush volume (i.e., washout) to the recovery of motor and sensory block in patients undergoing 2% lidocaine with epinephrine epidural anesthesia. METHODS: A prospective, randomized, double-blind study design was utilized. Thirty-three subjects scheduled for elective gynecologic or obstetrical surgical procedures underwent epidural anesthesia using 2% lidocaine with epinephrine (1:200,000). A T4 dermatome level of analgesia, determined by toothpick prick, was maintained intraoperatively. Following surgery, subjects were randomized to 1 of 3 treatment groups. Group 1 (control, n = 11) received no epidural 0.9% NaCl (normal saline [NS]) postoperatively. Group 2 (15 mL NS x 1, n = 10) received an epidural bolus of 15 mL NS. Group 3 (15 mL NS x 2, n = 12) received an epidural bolus of 15 mL NS postoperatively and a second 15-mL NS bolus 15 minutes later. Assessment of motor and sensory block was performed at 15-minute intervals until complete motor and sensory recovery. RESULTS: Times to partial and full motor and sensory recovery were significantly faster in the epidural NS groups than in the control group. Full motor recovery was more rapid in subjects receiving two 15-mL NS epidural NS boluses (30 mL total) compared with those receiving a single 15-mL NS bolus (108 +/- 9 min v 136 +/- 13 min) and significantly faster than control group subjects (153 +/- 14 min). Both NS x 1 and NS x 2 epidural bolus groups experienced significantly reduced times to complete sensory recovery when compared with the control group (NS x 1 = 154 +/- 13 min, NS x 2 = 153 +/- 9 min, control 195 +/- 14 min). CONCLUSIONS: A more rapid recovery of motor and sensory block in patients undergoing 2% lidocaine with epinephrine epidural anesthesia can be achieved with the use of 30 mL NS epidural washout. Reg Anesth Pain Med 2001;26:246-251.     

Caudal anesthesia with lidocaine or bupivacaine: plasma local anesthetic concentration and extent of sensory spread in old and young patients

Continuous caudal peridural anesthesia with 2% lidocaine (6 mg/kg) or 0.75% bupivacaine (2.2 mg/kg), both with epinephrine 1:200,000, was studied in two groups of male patients, younger than 40 or older than 55 yr old, respectively. Patients receiving lidocaine in the younger group (n = 6) were 32 +/- 5.2 (mean +/- SD) yr old and weighed 75 +/- 12 kg, while those in the older group (n = 16) were 66 +/- 5.3 yr old and weighed 72 +/- 8.2 kg. Patients receiving bupivacaine in the respective groups were 27 +/- 7.0 yr old (n = 5), and 76 +/- 10 kg compared to 69 +/- 10 yr (n = 14) and 75 +/- 10 kg. Anesthesia was satisfactory in all patients. Extent of sensory anesthesia, peak plasma lidocaine or bupivacaine concentrations, and area under the plasma concentration-time curves were independent of age. No local anesthetic toxicity was observed and peak drug concentrations were below those commonly associated with toxicity.     

Endogenous endothelin and vasopressin support blood pressure during epidural anesthesia in conscious dogs.

We studied whether endogenous endothelin, like endogenous vasopressin, helps to maintain blood pressure during high epidural anesthesia when efferent sympathetic drive is diminished. On different days, six awake dogs underwent each of the following five interventions: blockade of vasopressin V(1a) receptors using [d(CH(2))(5)Tyr(Me(2))]AVP, (40 microg/kg) or endothelin receptors using tezosentan (3 mg/kg followed by 3 mg. kg(-1). h(-1)) with or without epidural anesthesia (1% lidocaine, intraindividual dose did not differ between experiments), and epidural saline (n = 5). The effects of endothelin- or vasopressin-receptor blockade were analyzed (means +/- SEM) and compared by an analysis of variance for repeated measures (paired Student's t-test, alpha-adjusted, P < 0.05). Vasopressin-receptor blockade decreased blood pressure (10 +/- 2 mm Hg) only in the presence of epidural anesthesia, whereas endothelin-receptor blockade reduced blood pressure both in the presence and absence of epidural anesthesia (12 +/- 3 versus 10 +/- 1 mm Hg). During baseline and each intervention, plasma concentrations of vasopressin and big-endothelin were measured and compared by a Wilcoxon's rank sum test; P < 0.05. Vasopressin concentrations increased during epidural anesthesia and after additional endothelin receptor blockade, but big-endothelin concentrations remained unchanged during each intervention. We conclude that vasopressin acts as a reserve system, as it stabilizes blood pressure specifically during epidural anesthesia, whereas the unchanged concentrations of big-endothelin indicate that the endothelin system is not specifically activated to support blood pressure during epidural anesthesia. IMPLICATIONS: We studied in awake dogs whether endogenous endothelin, like endogenous vasopressin, helps to maintain blood pressure during resting conditions and epidural anesthesia. Only vasopressin was specifically activated to support blood pressure during epidural anesthesia, whereas endothelin supported blood pressure to the same extent during epidural anesthesia and during resting conditions.     

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

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

Halothane,isoflurane, and fentanyl increase the minimally effective defibrillation threshold of an implantable cardioverter defibrillator: first report in humans

Placing an implantable cardioverter defibrillator (ICD) involves the induction of ventricular fibrillation, whereupon the minimally effective defibrillation energy threshold (DFT) is determined. We evaluated the effects of 0.7% halothane, 1% isoflurane, or 1.5 micro g/kg of IV fentanyl during N(2)O/oxygen-based general anesthesia (GA) or those of subcutaneous 1.5% lidocaine plus IV 0.35 mg/kg of propofol on the DFT during ICD implantation in humans (n = 20 per group). Thirty minutes after the first set of DFT measurements under such conditions, the inhaled anesthetics were withdrawn, and all three GA groups received fentanyl 1 microg/kg IV (second set). A third set was taken 30 min later, before the GA patients awakened and when only N(2)O/oxygen was delivered for GA. The lidocaine plus propofol patients were given the same IV propofol bolus 1 min before each fibrillation/defibrillation trial and at the same time points as the three GA groups. The first DFTs were 16.1 +/- 2.2 J (halothane), 17.7 +/- 2.7 J (isoflurane), 16.4 +/- 2.9 J (fentanyl), and 12.9 +/- 3.8 J (lidocaine plus propofol) (P = 0.01). The second set of DFTs were significantly lower than the first sets for the halothane (P = 0.01) and isoflurane (P = 0.02), but not the fentanyl or lidocaine plus propofol, regimens. The third DFTs were significantly (P < 0.01) lower than the first ones for the three GA groups, but not for the lidocaine plus propofol patients. Thus, halothane, isoflurane, and fentanyl increased DFT values during ICD implantation in humans, whereas lidocaine plus intermittent small-dose IV propofol minimized these thresholds. IMPLICATIONS: Halothane, isoflurane, and IV fentanyl added to N(2)O/oxygen-based general anesthesia similarly increase minimal defibrillation threshold energy requirements (DFT) during cardioverter defibrillator implantation in humans. Subcutaneous lidocaine plus intermittent small-dose IV propofol minimizes DFT compared with these general anesthetics while providing equal patient satisfaction.     

Epidural clonidine suppresses the baroreceptor-sympathetic response depending on isoflurane concentrations in cats

Epidural administration of clonidine induces hypotension and bradycardia secondary to decreased sympathetic nerve activity. In this study, we sought to elucidate the change in baroreflex response caused by epidural clonidine. Thirty-six cats were allocated to six groups (n = 6 each) and were given either thoracic epidural clonidine 4 micro g/kg or lidocaine 2 mg/kg during 0.5, 1.0, or 1.5 minimum alveolar anesthetic concentration (MAC) isoflurane anesthesia. Heart rate (HR), mean arterial blood pressure (MAP), and cardiac sympathetic nerve activity (CSNA) were measured. Depressor and pressor responses were induced by IV nitroprusside 10 micro g/kg and phenylephrine 10 micro g/kg, respectively. Baroreflex was evaluated by the change in both CSNA and HR relative to the peak change in MAP (deltaCSNA/deltaMAP and deltaHR/deltaMAP, respectively). These measurements were performed before and 30 min after epidural drug administration. Epidural clonidine and lidocaine decreased HR, MAP, and CSNA by similar extents. deltaCSNA/deltaMAP and deltaHR/deltaMAP for depressor response were suppressed with epidural lidocaine and clonidine in all groups but the clonidine 0.5 MAC isoflurane group (0.197 +/- 0.053 to 0.063 +/- 0.014 and 0.717 +/- 0.156 to 0.177 +/- 0.038, respectively, by epidural lidocaine [P < 0.05] but 0.221 +/- 0.028 to 0.164 +/- 0.041 and 0.721 +/- 0.177 to 0.945 +/- 0.239, respectively, by epidural clonidine during 0.5 MAC isoflurane). Those for pressor response were suppressed in all groups. We conclude that thoracic epidural clonidine suppresses baroreflex gain during isoflurane anesthesia >1.0 MAC but may offer certain advantages compared with epidural lidocaine during 0.5 MAC isoflurane by virtue of preserving baroreflex sensitivity when inadvertent hypotension occurs.     

Does epidural anesthesia have general anesthetic effects? A prospective, randomized, double-blind, placebo-controlled trial

BACKGROUND: Clinically, patients require surprisingly low end-tidal concentrations of volatile agents during combined epidural-general anesthesia. Neuraxial anesthesia exhibits sedative properties that may reduce requirements for general anesthesia. The authors tested whether epidural lidocaine reduces volatile anesthetic requirements as measured by the minimum alveolar concentration (MAC) of sevoflurane for noxious testing cephalad to the sensory block. METHODS: In a prospective, randomized, double-blind, placebo-controlled trial, 44 patients received 300 mg epidural lidocaine (group E), epidural saline control (group C), or epidural saline-intravenous lidocaine infusion (group I) after premedication with 0.02 mg/kg midazolam and 1 microg/kg fentanyl. Tracheal intubation followed standard induction with 4 mg/kg thiopental and succinylcholine 1 mg/kg. After 10 min or more of stable end-tidal sevoflurane, 10 s of 50 Hz, 60 mA tetanic electrical stimulation were applied to the fifth cervical dermatome. Predetermined end-tidal sevoflurane concentrations and the MAC for each group were determined by the up-and-down method and probit analysis based on patient movement. RESULTS: MAC of sevoflurane for group E, 0.52+/-0.18% (+/- 95% confidence interval [CI]), differed significantly from group C, 1.18+/-0.18% (P < 0.0005), and from group I, 1.04+/-0.18% (P < 0.001). The plasma lidocaine levels in groups E and I were comparable (2.3+/-1.0 vs. 3.0+/-1.2 microg/ml +/- SD). CONCLUSIONS: Lidocaine epidural anesthesia reduced the MAC of sevoflurane by approximately 50%. This MAC sparing is most likely caused by indirect central effects of spinal deafferentation and not to systemic effects of lidocaine or direct neural blockade. Thus, lower concentrations of volatile agents than those based on standard MAC values may be adequate during combined epidural-general anesthesia.     

Optimum concentration of bupivacaine for combined caudal--general anesthesia in children

Caudal epidural anesthesia has become widely accepted as a means of providing postoperative pain relief and intraoperative supplementation to general anesthesia for children. To determine the best concentration of bupivacaine for combined general-caudal anesthesia in children, 122 children aged 1-8 yr scheduled for outpatient inguinal herniorrhaphy were randomized to receive, in a double-blind fashion, caudal anesthesia with bupivacaine in one of six concentrations (0.125, 0.15, 0.175, 0.2, 0.225, or 0.25%). After incision, a programmed reduction in inspired halothane resulted, if tolerated by the subject, in an inspired halothane concentration of 0.5% 10 min after incision. End-tidal halothane concentration at hernia sac ligation for subjects receiving 0.175% bupivacaine (0.55 +/- 0.03%) was less than that for subjects receiving 0.15% bupivacaine (0.75 +/- 0.05%; P less than 0.05). Subjects receiving 0.175% bupivacaine also were discharged earlier from the postanesthesia care unit (PACU) (27 +/- 1 min) than were subjects receiving 0.15% bupivacaine (38 +/- 5 min; P = 0.05). Children receiving greater than or equal to 0.2% bupivacaine tended to complain more of leg weakness after surgery; however, the difference did not reach statistical significance (39 of 67 vs. 16 of 47; P = 0.057). The incidence of complaints of leg weakness and paresthesia was positively correlated with bupivacaine concentration (r = 0.706; P = 0.05). Subjects receiving 0.125% bupivacaine had higher pain scores on arrival to the PACU than did those receiving 0.2% bupivacaine (P = 0.05); there were no other differences in pain scores.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical evaluation of clonidine added to lidocaine solution for epidural anesthesia

The effects of clonidine added to lidocaine solution used for epidural anesthesia were assessed in 92 women scheduled for surgery and premedicated with diazepam 10 mg po. Patients received 18 ml 2% lidocaine with clonidine 5 micrograms.ml-1 (group C-5, n = 26), with clonidine 10 micrograms.ml-1 (group C-10, n = 20), with epinephrine 5 micrograms.ml-1 (group E, n = 26), or plain (group P, n = 20). No significant difference in the number of segments of analgesia was found at any observation period among the four groups of patients. The decreases in mean blood pressure (BP) observed 20 min after epidural injection in those given clonidine (5 +/- 8% for C-5, 10 +/- 11% for C-10, mean +/- SD) were similar to those given plain lidocaine (7 +/- 12%) but significantly less than those given epinephrine (18 +/- 12%, P less than 0.01 vs. C-5 or P). The response of BP to ephedrine given for restoring BP during anesthesia was not attenuated in patients who received epidural clonidine. Heart rate (HR) decreased significantly in patients given clonidine 10 micrograms.ml-1 (7 +/- 8%, P less than 0.01), but not in those given clonidine 5 micrograms.ml-1, whereas HR increased significantly in those given lidocaine plain or with epinephrine (10 +/- 8% and 28 +/- 14%, respectively, P less than 0.01). The incidence of sinus bradycardia was similar among the four groups of patients. Significant differences were also observed in sedation score between clonidine groups and groups P or E; sedation appeared approximately 10-20 min after epidural injection in both clonidine groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Flumazenil improves cognitive and neuromotor emergence and attenuates shivering after halothane-, enflurane- and isoflurane-based anesthesia

PURPOSE: To conduct a randomized, placebo-controlled, double-blinded, clinical experiment testing the hypothesis that flumazenil, a benzodiazepine antagonist, may affect recovery from halothane-, enflurane- and isoflurane-based anesthesia. METHOD: Patients who underwent surgery under N(2)O/O(2) plus halothane (n=100), enflurane (n=100) or isoflurane (n=70) anesthesia were administered flumazenil 1 mg or placebo upon emergence from anesthesia, and their postanesthesia vital signs, vigilance, neurological recovery, shivering, amnesia reversal, and general subjective feeling were assessed. RESULTS: A ten-point vigilance score showed better recovery of flumazenil-treated patients compared to those who received placebo (60-min after halothane anesthesia: 9.9 +/- 0.1 vs 9.5 +/- 0.2, P <0.01; after enflurane: 10 +/- 0 vs 9.4 +/- 0.2, P <0.01; after isoflurane: 10.0 +/- 0 vs 9.3 +/- 0.1, P <0.01). Halothane- and enflurane-flumazenil-treated patients (but not isoflurane) reached a better neurological score (2.97 +/- 0.05 or 3 +/- 0) compared to placebo (2.8 +/- 0.4 or 2.6 +/- 0.4, P <0.01), respectively. Reversal of amnesia was superior in the flumazenil group at 60 min and at 24 hr postsurgery, and more flumazenil patients rated recovery as "pleasant". Flumazenil patients shivered less than placebo patients despite their lower core temperature (at 30 min: halothane: 11% vs 28%, P <0.05; enflurane: 11% vs 30%, P <0.05; isoflurane: 17% for both groups). CONCLUSION: Flumazenil improves recovery of high cortical and neuromotor functions following halothane, enflurane and isoflurane anesthesia, reduces shivering and improves the overall quality of emergence, including patients' subjective feeling.     

The effects of intravenous lidocaine administration on the minimum alveolar concentration of isoflurane in cats

Lidocaine decreases the minimum alveolar concentration (MAC) of inhaled anesthetics and has been used clinically to reduce the requirements for other anesthetic drugs. In this study we examined the effects of lidocaine on isoflurane MAC in cats. Six cats were studied. In Experiment 1, the MAC of isoflurane was determined. An IV bolus of lidocaine 2 mg/kg was then administrated and venous plasma lidocaine concentrations were measured to determine pharmacokinetic values. In Experiment 2, lidocaine was administered to achieve target plasma concentrations between 1 and 11 microg/mL and the MAC of isoflurane was determined at each lidocaine plasma concentration. Actual lidocaine plasma concentrations were 1.06 +/- 0.12, 2.83 +/- 0.39, 4.93 +/- 0.64, 6.86 +/- 0.97, 8.86 +/- 2.10, and 9.84 +/- 1.34 microg/mL for the target concentrations of 1, 3, 5, 7, 9, and 11 microg/mL, respectively. The MAC of isoflurane in this study was 2.21% +/- 0.17%, 2.14% +/- 0.14%, 1.88% +/- 0.18%, 1.66% +/- 0.16%, 1.47% +/- 0.13%, 1.33% +/- 0.23%, and 1.06% +/- 0.19% at lidocaine target plasma concentrations of 0, 1, 3, 5, 7, 9, and 11 microg/mL, respectively. Lidocaine, at target plasma concentrations of 1, 3, 5, 7, 9, and 11 microg/mL, linearly decreased isoflurane MAC by -6% to 6%, 7% to 28%, 19% to 35%, 28% to 45%, 29% to 53%, and 44% to 59%, respectively. We conclude that lidocaine decreases the MAC of isoflurane.     

The number of injections does not influence local anesthetic absorption after paravertebral blockade

PURPOSE: The aims of this study are to determine if the injection of a single large dose of local anesthetics into the paravertebral space increases the risks of inducing toxicity compared with multiple small injections and to describe ropivacaine plasma concentrations resulting from paravertebral blockade. METHODS: Paravertebral blockade was performed using a solution of 10 mL ropivacaine 0.75%, 10 mL lidocaine CO2 2% plus 0.1 mL epinephrine 1:1000 either by a single injection at T3 or T4 (Group S, n = 6) or by five injections of 4 mL each at T2 to T6 (Group M, n = 8). Blood samples were taken at zero, five, ten, 15, 20, 30, 45, 60 and 90 min and at two, three, four, five, six and eight hours. Ropivacaine and lidocaine plasma concentrations were measured by high performance liquid chromatography. RESULTS: Maximal plasma concentrations were comparable for lidocaine: 2.6 +/- 1.3 (S) vs 2.6 +/- 0.8 microg x mL(-1) (M) and for ropivacaine: 1.3 +/- 0.2 (S) vs 1.3 +/- 0.1 microg x mL(-1) (M). Area under the plasma concentration-time curve was higher in Group M for lidocaine: 577.6 +/- 146.1 vs 401.7 +/- 53.2 mg x min(-1) x mL(-1) (P = 0.04) but similar for ropivacaine: 381.1 +/- 95.4 (M) vs 363.1 +/- 85.3 mg x min(-1) x L(-1) (S). CONCLUSIONS: The injection of a single large bolus of local anesthetics into the paravertebral space does not increase its absorption. Maximal ropivacaine plasma concentrations resulting from paravertebral blockade are similar to those reported with equivalent doses of bupivacaine.     

The anticonvulsant effects of volatile anesthetics on lidocaine-induced seizures in cats

Large concentrations of sevoflurane and isoflurane, but not halothane, induce spikes in the electroencephalogram. To elucidate whether these proconvulsant effects affect lidocaine-induced seizures, we compared the effects of sevoflurane, isoflurane, and halothane in cats. Fifty animals were allocated to 1 of 10 groups: 70% nitrous oxide (N2O), 0.6 minimum alveolar anesthetic concentration (MAC) + 70% N2O, 1.5 MAC + 70% N2O, and 1.5 MAC of each volatile agent in oxygen. Lidocaine 4 mg x kg(-1) x min(-1) was infused IV under mechanical ventilation with muscle relaxation. Electroencephalogram in the cortex, amygdala, and hippocampus and multiunit activities in the midbrain reticular formation (R-MUA) were recorded. Lidocaine induced spikes first from the amygdala or hippocampus in the 70% N2O and halothane groups and from the cortex in the sevoflurane and isoflurane groups. Lidocaine induced seizures in all cats in the 70% N2O and 0.6 MAC + N2O groups. Seizure occurrence was reduced in the 1.5 MAC + N2O group (P < 0.05 versus 70% N2O). The onset of seizure was delayed in the 0.6 MAC + N2O and 1.5 MAC groups for sevoflurane and isoflurane, but not for halothane, compared with the 70% N2O group (P < 0.05). Lidocaine increased R-MUA with seizure by 130%+/-56% in the 70% N2O group. The increase of R-MUA with seizure was more suppressed in the volatile anesthetic groups than in the 70% N2O group (P < 0.05). In the present study, sevoflurane and isoflurane attenuated seizure when the blood lidocaine concentration was accidentally increased. IMPLICATIONS: Increasingly, epidural blockade is combined with general anesthesia to achieve stress-free anesthesia and continuous pain relief in the postoperative period. In the present study, sevoflurane and isoflurane attenuated seizure when the blood lidocaine concentration was accidentally increased.