The effect of remifentanil on seizure duration and acute hemodynamic responses to electroconvulsive therapy

We designed this prospective, randomized, double-blinded, placebo-controlled, crossover study to evaluate the effect of different doses of remifentanil on the acute hemodynamic response and duration of seizure activity after a standardized electroconvulsive therapy (ECT) stimulus. Twenty consenting patients with major depressive disorders receiving maintenance ECT participated in this study. Eighty ECT treatments were evaluated. All patients were premedicated with glycopyrrolate 0.2 mg IV, unconsciousness was induced with methohexital 1 mg/kg IV, and muscle paralysis was produced with succinylcholine 1.2 mg/kg IV. Subsequently, patients received 1 of 3 different doses of remifentanil 25, 50, and 100 microg or saline (control) in a random sequence immediately after methohexital at 4 consecutive ECT treatments. Labetalol, in 5-mg IV boluses, was used as a rescue antihypertensive medication. A fixed suprathreshold electrical stimulus was administered to elicit a seizure, and the times from the stimulus to the cessation of the motor and electroencephalographic (EEG) seizure activity were noted. Pre- and post-ECT blood pressure values were significantly decreased in the 100- microg remifentanil group compared with the control group. The durations of motor (38 +/- 9 s to 43 +/- 15 s) and EEG (55 +/- 29 s to 60 +/- 21 s) seizure activity were not significantly different among the four groups. Similarly, recovery times to eye opening, obeying commands, and discharge from the recovery room did not differ among the four study groups. The requirement for labetalol after ECT was nonsignificantly decreased in the remifentanil groups. In conclusion, remifentanil 100 microg IV attenuated the acute hemodynamic response to ECT. Furthermore, remifentanil had no adverse effect on the duration of ECT-induced seizure activity. Finally, adjunctive use of remifentanil did not prolong recovery times or increase post-ECT side effects. IMPLICATIONS: Remifentanil (100 microg IV) attenuated the acute hemodynamic response after electroconvulsive therapy (ECT) without adversely affecting the length of the ECT-induced seizure activity or prolonging recovery times.     

Electromyographic assessment of ulnar nerve motor block induced by lidocaine

Study Objective: To determine the differences in the onset time and duration of motor block produced by lidocaine 1% and lidocaine 2% via a quantitative and objective method, the measurement of compound muscle action potentials (CMAPs).

Study Design: Prospective study.

Setting: Main operating rooms of a university hospital.

Patients: 20 consecutive patients undergoing surgery not requiring intraoperative muscle relaxation.

Interventions: General anesthesia with unilateral ulnar nerve block was administered. In patients’ nondominant (experimental) arms, an insulated block needle was placed adjacent to the ulnar nerve at the wrist while continuous nerve stimulation was delivered to ensure its proper placement. Through this needle, lidocaine 1% or lidocaine 2% was injected. The dominant (control) arm received no injection.

Measurements and Main Results: Monitoring of ulnar nerve-evoked CMAPs was performed simultaneously on both arms. Ulnar nerve function was assessed at baseline and then at 10-second intervals by automatically measuring the amplitude of the evoked CMAPs on a two-channel electromyogram. The mean (± SEM) baseline CMAP amplitude prior to injection of lidocaine 1% was 3.10 ± 0.87 mV and 3.06 ± 0.89 mV for the experimental and control ulnar nerves, respectively (p = NS); for lidocaine 2%, baseline CMAP amplitude was 3.58 ± 1.39 mV and 3.70 ± 1.46 mV, respectively (p = NS). Over the course of the study, the control CMAP amplitude varied by <12%. At the experimental ulnar nerve, 90% CMAP decrease after injection of lidocaine 1% and lidocaine 2% occurred 7.5 ± 2 minutes and 5 ± 1.5 minutes, respectively (p = NS), whereas maximal blockade was achieved after 15 ± 3 minutes and 11 ± 5 minutes, respectively (p = NS). Recovery of CMAP to 90% of baseline occurred 184 ± 31 minutes after injection of lidocaine 1% and 248 ± 30 minutes following lidocaine 2% (p = NS).

Conclusion: The present study describes a technique that can be used in vivo to objectively measure the speed of onset and duration of local anesthetic-induced motor blockade. Although statistically not different, lidocaine 2% demonstrated a faster onset and longer duration of ulnar nerve motor block than lidocaine 1%.     

Prevention of the cardiovascular and neuroendocrine response to electroconvulsive therapy: I. Effectiveness of pretreatment regimens on hemodynamics

Electroconvulsive therapy (ECT) under anesthesia is associated with hypertension and tachycardia. The cardiovascular effects of ECT were studied after pre-treatment of 10 patients with esmolol (1.0 mg/kg), fentanyl (1.5 micrograms/kg), labetalol (0.3 mg/kg), lidocaine (1.0 mg/kg), and saline solution (control), using a double-blind, randomized block-design. Each patient received all five pretreatment regimens over the course of five ECT sessions. During control studies, arterial blood pressure and heart rate increased significantly in all patients after ECT (P less than 0.05 and P less than 0.01, respectively). The rate-pressure product increased by an average of 336% +/- 14% (P less than 0.01). There were appreciable individual differences in the cardiovascular response to ECT, independent of pretreatment (P less than 0.01). Pretreatment with esmolol and labetalol significantly reduced the hemodynamic response to ECT, compared with fentanyl, lidocaine, or saline solution (P less than 0.05). Esmolol attenuated arterial blood pressure to a larger extent than did labetalol (P less than 0.05). Compared with saline solution (control), pretreatment with labetalol, fentanyl, or lidocaine significantly reduced seizure duration (P less than 0.05) and increased the frequency with which a second electrical stimulus was required. In contrast, esmolol pretreatment did not significantly affect seizure duration. Esmolol (1 mg/kg), administered 1 min before induction of anesthesia, produced significant amelioration of the cardiovascular response to ECT with minimal effect on seizure duration.     

Dexmedetomidine blunts acute hyperdynamic responses to electroconvulsive therapy without altering seizure duration

Background: This study was designed to evaluate the effect of dexmedetomidine on the acute hyperdynamic response, duration of seizure activity and recovery times in patients undergoing electroconvulsive therapy (ECT).
Methods: Fourteen patients underwent a total of 84 ECT sessions as a crossover design. Patients were randomly allocated to receive either dexmedetomidine (1 μg/kg IV over a period of 10 min) or saline (control). Anaesthesia was induced with propofol 1 mg/kg, and then succinylcholine 0.5 mg/kg IV was administered. Arterial blood pressure and heart rate (HR) were recorded during the study period.
Results: HR in the dexmedetomidine group was lower than that in the control group at 5 and 10 min after the start of study drug infusion, and at 1, 3 and 10 min after the seizure ended ( P <0.05). Peak HR was lower in the dexmedetomidine group compared with that in the control group ( P <0.05). The mean arterial pressure (MAP) values in the dexmedetomidine group were lower at 0, 1, 3 and 10 min after the seizure ended compared with the control group ( P <0.05). Both motor and electroencephalography (EEG) seizure duration in the control group (35.65 ± 14.89 and 49.07 ± 9.94 s, respectively) were similar to that in the dexmedetomidine group (33.30 ± 12.01 and 45.15 ± 17.79 s, respectively) ( P >0.05). Time to spontaneous breathing, eye opening and obeying commands were not different between the groups.
Conclusion: A dexmedetomidine dose of 1 μg/kg IV administered over 10 min before the induction of anaesthesia with propofol may be useful in preventing the acute hyperdynamic responses to ECT without altering the duration of seizure activity and recovery time.     

Dexmedetomidine Failed to Block the Acute Hyperdynamic Response to Electroconvulsive Therapy

Background: Orally administered clonidine (0.2-0.3 mg) has been reported to decrease the acute hypertensive response to electroconvulsive therapy (ECT) without prolonging early recovery. covery. This preliminary study was designed to evaluate the acute hemodynamic effects of the investigational [small alpha, Greek]2-adrenergic agonist, dexmedetomidine, in patients undergoing a series of ECT treatments.

Methods: Six patients undergoing a series of three to six consecutive ECT treatments were studied according to a randomized, double-blind, placebo-controlled protocol. All patients received either saline or dexmedetomidine, 0.5 or 1.0 [micro sign]g/kg intravenously, 10-30 min before induction of anesthesia for ECT using a standardized anesthesia protocol. In addition to assessing the cardiovascular variables, the duration of seizure activity, degree of sedation, and time to discharge from the Phase I recovery unit were assessed.

Results: Although dexmedetomidine produced dose-related increases in the level of sedation before the ECT procedure, it failed to decrease the peak blood pressure and heart rate responses after the ECT treatment. The 0.5 and 1.0 [micro sign]g/kg doses of dexmedetomidine prolonged the times to orientation and to discharge from the Phase I unit.     

Can the bispectral index be used to predict seizure time and awakening after electroconvulsive therapy?

The electroencephalogram (EEG) bispectral index (BIS) measures the hypnotic component of the anesthetic state and correlates with emergence from general anesthesia. Therefore, we hypothesized that the BIS would be useful in predicting electroconvulsive therapy (ECT)-induced seizure times and awakening from methohexital anesthesia. Twenty-five consenting patients with major depressive disorders underwent 100 maintenance ECT treatments. All patients were premedicated with glycopyrrolate 0.2 mg IV, and anesthesia was induced with methohexital 1 mg/kg IV. The BIS was monitored continuously, and the values were recorded at specific end-points, including before anesthesia (baseline), after the induction of anesthesia (pre-ECT), at the end of ECT (peak), after ECT (suppression), and on awakening (eye opening). The pre-ECT BIS value correlated with the duration of both the motor (r = 0.3) and EEG (r = 0.4) seizure activity (P < 0.05). The peak post-ECT BIS value correlated with the duration of the EEG seizure activity (r = 0.5) (P < 0.05). A positive correlation was also found between the EEG seizure duration and the time to eye opening (r = 0.4) (P < 0.05). However, the BIS values on awakening from methohexital anesthesia varied from 29 to 97 and were <60 in 75% of the cases. We conclude that the BIS value before the ECT stimulus is applied could be useful in predicting the seizure time. However, the BIS values on awakening were highly variable, suggesting that it reflects both the residual depressant effects of methohexital and post-ictal depression. IMPLICATIONS: The bispectral index (BIS) value immediately before the electroconvulsive therapy (ECT) stimulus correlates with the duration of the motor and electroencephalogram (EEG) seizure activity during methohexital anesthesia. In addition, the increase in the BIS value during the ECT-induced seizure was proportional to the duration of EEG seizure activity. However, the BIS value on awakening from anesthesia varied widely, from 29 to 97.     

Combined popliteal and posterior cutaneous nerve of the thigh blocks for short saphenous vein stripping in outpatients: An alternative to spinal anesthesia

Study Objective: To compare a combination of peripheral nerve blocks with spinal anesthesia in ambulatory patients undergoing short saphenous vein stripping.

Design: Prospective, randomized study.

Setting: University hospital.

Patients: 28 ASA physical status I and II ambulatory surgery patients undergoing short saphenous vein stripping.

Interventions: 14 patients received a popliteal block (sciatic nerve block at the popliteal fossa) using 30 ml of alkalinized 3 % chloroprocaine and a posterior cutaneous nerve of the thigh block with 10 ml of 1% lidocaine. The 14 patients who were randomized to the spinal anesthesia group received 65 mg of 5% hyperbaric lidocaine.

Measurements and Main Results: There were no significant differences in age and gender between the two groups (mean age 53 ± 13 years, 8 men and 20 women). Patients in the peripheral nerve block group recovered significantly faster in phase 1 of the postanesthesia care unit (PACU) (67 ± 10 min vs. 122 ± 50 min, p < 0.01) and were discharged home sooner (222 ± 53 min vs. 294 ± 69 min, p < 0.01) than the patients in the spinal anesthesia group.

Conclusions: The combination of popliteal and posterior cutaneous nerve of the thigh blocks provided adequate anesthesia and a faster recovery profile with a similar subjective acceptance of both anesthetic techniques in ambulatory patients undergoing short saphenous vein stripping in the prone position.     

The timing of electroconvulsive therapy and bispectral index after anesthesia induction using different drugs does not affect seizure duration

STUDY OBJECTIVE: To determine the association between bispectral index (BIS) and seizure duration obtained by electroconvulsive therapy (ECT) administered sooner or later after anesthetic induction. DESIGN: Prospective, randomized, crossover study. SETTING: University-affiliated medical center. PATIENTS: Nine ASA physical status I, II, and III patients undergoing a total of 31 ECTs. INTERVENTIONS: ECT was administered soon (<210 sec) or later (between 210 sec and 360 sec) after anesthetic induction. In each individual patient, drug regimens and ECT machine settings were identical. MEASUREMENTS: BIS immediately before the start of the ECT and the duration of the EEG seizure were recorded, as well as the time period between loss of consciousness and ECT administration. MAIN RESULTS: There was no relationship between BIS level and seizure duration. Moreover, seizure duration was not dependent on the time of ECT administration in the time window between one and 6 minutes after loss of consciousness. CONCLUSION: The hypnotic drug effect measured by the BIS is not correlated to the seizure duration obtained by ECT.     

The use of nicardipine for electroconvulsive therapy: a dose-ranging study

A wide variety of vasoactive drugs have been used to treat the acute hypertensive response to electroconvulsive therapy (ECT). We designed this randomized, double-blind, saline-controlled, crossover study to compare three different doses of nicardipine when administered before the ECT stimulus. Twenty-five patients undergoing a series of 4 ECT treatments received bolus injections of either saline or nicardipine 20, 40, or 80 mug/kg IV in a random sequence during a standardized methohexital (1 mg/kg) and succinylcholine (1 mg/kg) anesthetic technique. The mean arterial blood pressure (MAP) and heart rate values were recorded at specific time intervals, as were the duration of seizure activity and the need for rescue labetalol. Both the 40 and 80 mug/kg doses of nicardipine reduced the percentage increase in MAP above the baseline value compared with the saline group (7% and 7% versus 30%, respectively). Nicardipine 40 and 80 mug/kg were also associated with a significant reduction in the need for labetalol (7 +/- 3 mg and 5 +/- 0 mg versus 22 +/- 10 mg in the saline group). Compared with the 40 mug/kg dose, nicardipine 80 mug/kg was associated with a more rapid heart rate at the time the ECT stimulus was applied. The 80 mug/kg dose was also associated with a reduced MAP value on awakening compared with the baseline value (91 +/- 12 mm Hg versus 102 +/- 8 mm Hg). We conclude that a bolus injection of nicardipine 40 mug/kg IV immediately before the ECT stimulus was optimal for controlling the acute hemodynamic response to ECT treatments.     

Midazolam does not antagonize fentanyl-mediated analgesia in surgical patients

Study Objective: To determine whether midazolam possesses a clinically significant antianalgesic action in surgical patients.

Design: Randomized, controlled study.

Setting: Inpatient anesthesia at a university department of neurosurgery.

Patients: 2 groups of 10 patients each who were scheduled for supratentorial brain surgery, did not have elevated intracranial pressure, and were free from systemic disease.

Interventions: Patients underwent anesthesia induction with hexobarbital, succinylcholine, and pancuronium; anesthesia was maintained with injections of droperidol fentanyl (Group 1) or with midazolam fentanyl (Group 2) following a predetermined repetitive dosing schedule, such that fentanyl 0.1 mg was injected upon predominant increases in heart rate, whereas droperidol 2.5 mg or midazolam 2.5 mg was injected upon increases in blood pressure.

Measurements and Main Results: Duration of anesthesia and invasiveness of surgery were similar in both groups. The amount of fentanyl required was 0.55 ± 0.18 mg/hr (mean ± SD) in Group 1 and 0.53 ± 0.17 mg/hr in Group 2. Injections of droperidol 7.5 ± 3.4 mg/hr (Group 1) and midazolam 5.9 ± 2.3 mg/hr (Group 2) were administered intraoperatively. This redosing regimen was associated with uninterrupted hemodynamic stability, indicating comparable and adequate anesthetic depth. Plasma concentrations of metabolites and hormones indicative of humoral stress activation did not differ between groups.

Conclusion: Under these clinical conditions, the administration of midazolam, when compared with droperidol, was not associated with signs of any antagonistic or antianalgesic action toward fentanyl-mediated analgesia.     

Sympathetic Nervous System Response to Lidocaine Induced Seizures in Cats

The effect on arterial pressure, EEG, preganglionic sympathetic nervous activity and pulse rate of repeated intravenous administrations of lidocaine (3 mg/kg) was investigated in cats anaesthetized with nitrous oxide. A continuous high voltage, burst-suppression EEG indicating constant seizure activity was found, whereas arterial pressure and sympathetic nervous activity did not change significantly. Although the onset of EEG seizure activity did not change the mean sympathetic activity level, the pattern of firing changed dramatically as every EEG seizure triggered a burst of sympathetic impulses. Barostatic reflexes were active after lidocaine administration unless seizure activity occurred. Thiopental 5 mg/kg given intravenously to cats during continuous lidocaine-induced EEG seizures always abolished the seizure activity without excessive depression of arterial pressure.     

Transcutaneous Electrical Nerve Stimulation Does Not Augment Epidural Labor Analgesia

Study Objective: To evaluate whether transcutaneous electrical nerve stimulation (TENS) can increase the quality and duration of an initiation dose of bupivacaine used for the establishment of epidural labor analgesia.

Design: Randomized, double-blind study.

Setting: Tertiary-care academic medical center.

Patients: 40 ASA physical status I and II parturients in early, active spontaneous labor with a singleton, vertex term fetus, and requesting analgesia.

Interventions: A standardized epidural technique with either an active or inactive TENS unit was performed. Before epidural placement, TENS intensity thresholds were determined with electrodes placed over the paraspinus muscles at T₁₀–L₁, and S₂–S₄; TENS settings for mode, cycle, and pulse width were standardized.

Measurements: Data were collected at timed intervals on pain as measured by visual analog scale (VAS), sensory level (pinprick), motor blockade (Bromage score), cervical dilation, and duration of analgesia.

Main Results: The duration of analgesia produced by the initial dose of epidural bupivacaine did not differ between groups (TENS turned off 82.3 ± 26 [mean ± SD] vs. TENS activated 80.7 ± 40 min, p = 0.88). Kaplan-Meier survival analysis and Mantel-Cox log rank analysis showed no difference between the two treatments (p = 0.75). No difference in the quality of analgesia was observed between the two groups.

Conclusions: In healthy laboring parturients, the application of a TENS unit did not alter the quality or duration of an initiation dose of bupivacaine utilized for the establishment of epidural labor analgesia.     

Subarachnoid bupivacaine blockade decreases midazolam and thiopental hypnotic requirements

Study Objective: To test the hypothesis that subarachnoid bupivacaine blockade decreases hypnotic requirements for thiopental sodium and midazolam.

Design: Randomized, double-blind, placebo-controlled study.

Setting: Teaching hospital.

Patients: 53 nonpremedicated ASA physical status I and II adult male patients scheduled for elective lower abdominal, pelvic, or lower limb surgery.

Interventions: Intravenous injections of midazolam or thiopental were administered with or without subarachnoid bupivacaine blockade (12.5 mg) at the L₃–L₄ level. Thiopental or midazolam hypnotic requirements were determined using loss of ability to open eyes in response to verbal command as an endpoint. The thiopental requirements were determined by titration; the midazolam requirements were determined from dose-response curves obtained with bolus injections of predetermined doses of the drug.

Measurements and Main Results: Subarachnoid bupivacaine blockade decreased the hypnotic dose of thiopental from 3.40 ± 0.68 mg/kg (mean ± SD) with a dose range of 2.3 to 4.5 mg/kg (intramuscular saline) to 2.17 ± 0.48 mg/kg with a dose range of 1.3 to 2.8 mg/kg (p < 0.005 for the difference). The ED₅₀ value of midazolam decreased with the bupivacaine blockade, from 0.23 mg/kg (95% confidence limits: 0.08 to 0.38 mg/kg) to 0.06 mg/kg (0.01 to 0.14 mg/kg), with p < 0.0001 for the difference.

Conclusion: Subarachoid bupivacaine blockade decreases hypnotic requirements for both thiopental and midazolam. The results suggest that the reduction in hypnotic requirements is due to the decrease in afferent input induced by spinal anesthesia.     

Ketamine, Not Propofol, Attenuates Cerebrovascular Response to Carbon Dioxide in Humans With Isoflurane Anesthesia

Study Objectives: To investigate the effects of ketamine and propofol on the cerebrovascular response to carbon dioxide (CO₂) in humans during isoflurane anesthesia.

Design: Randomized clinical investigation.

Settings: University hospital of a medical school.

Patients: 30 ASA physical status I and II adult, elective surgical patients.

Interventions and Measurements: With each patient given air/oxygen/isoflurane anesthesia, the flow velocity in the middle cerebral artery (Vmca) and pulsatility index were measured using the transcranial Doppler method under hypocapnic [arterial CO₂tension (Pa ₂) 28–32 mmHg], normocapnic (Pa ₂ 38–42 mmHg), and hypercapnic conditions (Pa ₂ 48–52 mmHg). Pa ₂ was altered by supplementing the inspired gas with CO₂ without changing the respiratory conditions. Patients were then randomly assigned to receive either ketamine 1 mg · kg⁻¹ or propofol (2 mg · kg⁻¹followed by an infusion of 6–10 mg · kg⁻¹ · hr⁻¹) (n = 15 for each drug), and the measurements were repeated.

Main Results: Ketamine reduced both absolute and relative cerebrovascular reactivity to CO₂ significantly [2.9 ± 0.8 (control) vs. 2.6 ± 1.0 (ketamine) cm · sec⁻¹ · mmHg⁻¹: p < 0.05; and 3.5 ± 0.7 (control) vs. 2.8 ± 0.9 (ketamine) % · mmHg⁻¹: p < 0.01, respectively]. However, ketamine did not reduce Vmca during hypercapnic conditions (117 ± 29 cm · sec⁻¹) compared with controls (120 ± 28 cm · sec⁻¹). Although propofol decreased Vmca during all conditions, it did not cause any change in either absolute or relative CO₂ reactivity [2.5 ± 0.8 (control) vs. 2.5 ± 1.0 (propofol) cm · sec⁻¹ · mmHg⁻¹, and 3.3 ± 1.3 (control) vs. 4.1 ± 1.0 (propofol) % · mmHg⁻¹, respectively].

Conclusions: In humans given isoflurane anesthesia, a) ketamine reduced cerebrovascular response to CO₂, but cerebral blood flow (CBF) during hypercapnic conditions was comparable with controls, and b) although propofol decreases CBF, it maintains the cerebrovascular response to CO₂.     

Effect of methohexitone and propofol with or without alfentanil on seizure duration and recovery in electroconvulsive therapy

We have studied the effects of methohexitone and propofol with and without alfentanil on seizure duration and recovery in this observer- blinded, prospective, randomized, crossover study involving 24 patients undergoing electroconvulsive therapy (ECT). Each patient had four treatment sessions, and received the following four i.v. regimens in random order: methohexitone 0.75 mg kg-1, methohexitone 0.50 mg kg-1 and alfentanil 10 micrograms kg-1, propofol 0.75 mg kg-1, propofol 0.50 mg kg-1 and alfentanil 10 micrograms kg-1. Additional methohexitone or propofol was given as needed in 10-20-mg increments until loss of consciousness. Suxamethonium 1.0 mg kg-1 i.v. was given for muscular paralysis. Mean motor and EEG seizure durations were longer with methohexitone-alfentanil (44.7 (SD 15.0) and 70.5 (29.7) s) than with methohexitone (37.6 (12.6) and 52.6 (15.3) s) and similarly, seizures were longer with propofol-alfentanil (36.8 (15.2) and 54.5 (20.9) s) than with propofol alone (27.2 (11.9) and 39.2 (3.9) s). Seizures were longest with methohexitone-alfentanil and shortest with propofol. Recovery time was statistically shorter in patients receiving propofol compared with methohexitone-alfentanil and methohexitone alone. Alfentanil with a reduced dose of methohexitone or propofol provided unconsciousness and increased seizure duration in patients undergoing ECT. We conclude that the combination of methohexitone with alfentanil is a good regimen for ECT, especially for patients with short seizure duration.      

Lidocaine-induced hemodynamic effects are enhanced by the inhibition of endothelium-derived relaxing factor in dogs

Background: Lidocaine has been shown to have direct vasoconstrictive effects at low concentrations. Since lidocaine inhibits endothelium-dependent vasodilation in vitro , the vasoconstrictor effect of lidocaine may be due to inhibition of endothelium-derived relaxing factor(EDRF/NO). Therefore, the current study was designed to determine the effects of N^G-nitro-L-arginine (L-NNA), a potent inhibitor of nitric oxide synthase, on systemic and pulmonary hemodynamics during lidocaine infusion.
Methods: Systemic and pulmonary hemodynamic effects of lidocaine infusion, 1 mg kg^-1 min^-1, for 10 min were measured in dogs anesthetized with 1% halothane in oxygen. Dogs were studied twice with an interval of 1 week in a cross-over study, and were assigned to one of two groups that received saline or L-NNA intravenously in group 1 (n=8), or L-NNA or L-NNA+L-arginine which reverses the nitric oxide synthesis inhibitor effect of L-NNA, intravenously in group 2 (n=8) prior to lidocaine infusion. The free serum concentration of and protein-binding ratio for lidocaine were measured.
Results: With saline pretreatment in group 1, lidocaine infusion significantly decreased cardiac index (CI) and significantly in-
Conclusion: In contrast to in vitro study, vasoconstrictor effect of lidocaine is enhanced when a capacity for compensatory vasodilation including EDRF/NO pathway is exhausted in halo-thane-anesthetized dogs.     

Effect of divided supplementation of remifentanil on seizure duration and hemodynamic responses during electroconvulsive therapy under propofol anesthesia

Purpose

Although a reduced dose of propofol combined with remifentanil is often used in anesthesia for electroconvulsive therapy (ECT), there have been few studies in which the optimal technique for injection of remifentanil was examined in detail. The aim of this study was to evaluate the effects of single and divided injection of remifentanil combined with propofol on seizure duration and hemodynamic responses during ECT.

Methods

Twenty-six ASA I?CII patients were enrolled in this study and received a total of 78 ECTs. Each patient received propofol 1.2?mg/kg (group P), remifentanil 1???g/kg followed by propofol 0.5?mg/kg (group R1), and remifentanil 1???g/kg followed by propofol 0.5?mg/kg and thereafter remifentanil 2???g/kg (group R2). Succinylcholine 1?mg/kg was used for muscle paralysis after loss of consciousness.

Results

Although mean motor seizure durations were significantly longer in groups R1 and R2 than in group P (P?P?P?Conclusions Divided use of remifentanil at 1 and 2???g/kg combined with propofol 0.5?mg/kg produces an acceptable outcome in both seizure duration and hemodynamic stability during ECT compared with the standard hypnotic doses of propofol alone or remifentanil 1???g/kg followed by propofol 0.5?mg/kg.     

Topographical analysis of the EEG effects of a subconvulsive dose of lidocaine in healthy volunteers

Background: The purpose of the present study was to assess the effects of intravenous lidocaine on spatial changes of electroen-cephalographic power and on psychomotoric status in conscious volunteers.
Methods: In 11 healthy volunteers lidocaine (2-min bolus, 100 mg; 15-min infusion, 40 μg kg^-1 min^-1) or placebo were given intravenously in a randomized, single-blinded, two-way crossover study. Haemodynamics and lidocaine plasma concentrations were measured at baseline and within a period of 30 min following bolus injection. Vigilance and emotional status were tested using visual analogue scales (VAS). Toxic CNS effects were evaluated by a questionnaire. The raw EEG (17 leads, reference C_z) and computed power spectra were continuously recorded.
Results: The chosen lidocaine dosage led to nearly constant plasma concentrations (unbound lidocaine 2.5 min and 15 min after bolus 0.36±0.14 μg/ml and 0.30±0.06 μg/ml, respectively [mean±SD]). The placebo caused no symptoms, changes in VAS-scores or EEG-parameters. Lidocaine induced pronounced subjective symptoms and significant increases in delta activity for 15 min, most dominant at the frontotemporal and occipital leads (max. +219% O₁). Frontal and occipital beta1 and beta2 power (max. +131% and +124% at O₁, respectively) was immediately increased after the bolus injection. No EEG changes occurred at central region C_z, and no interhemispheric EEG differences were noted. Theta, alphal, and alpha2 power remained unchanged.
Conclusion: The current data demonstrate simultaneous changes in psychomotoric status as well as delta and beta spectral power during lidocaine infusion. These data could be an indication that the pronounced frontotemporal and occipital EEG changes are the electroencephalographic expression of subjective sensations.     

Effects of combined methohexitone-remifentanil anaesthesia in electroconvulsive therapy

BACKGROUND: Methohexitone is widely used to provide anaesthesia for patients undergoing electroconvulstive therapy (ECT). Short seizure duration, high blood pressures (BP) and heart rates (HR) are usual in elderly patients. In this study, elderly patients undergoing ECT received low dose methohexitone with remifentanil or methohexitone alone and motor seizure duration, haemodynamic response and recovery time were compared. METHODS: Ten patients, of mean age 74.3 years, were enrolled in this double-blind, randomised crossover trial, receiving a total of 38 ECTs. Each patient was given the following two i.v. regimens in random order: A) methohexitone 0.5 mg kg(-1) combined with remifentanil 1.0 microg kg(-1) and B) methohexitone 0.75 mg kg(-1). Additional methohexitone was given, if needed, until loss of consciousness, and then suxamethonium 1.0 mg kg(-1) for muscular paralysis. RESULTS: Mean motor seizure duration was significantly longer with methohexitone-remifentanil (37.6 s (SD 12.0)) than with methohexitone alone (27.1 (SD11.5)) (P=0.0009). Recovery time, time to spontaneous breathing, peak postictal changes in BP and HR were similar with both regimens. CONCLUSION: A reduced dose of methohexitone combined with remifentanil allows prolonged duration of motor seizures in ECT. We conclude that low dose methohexitone combined with a short-acting opioid is a reasonable alternative for elderly patients undergoing ECT, and for other patients with short seizure duration.     

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

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