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Electroconvulsive therapy is an effective treatment for severe and medication-resistant depression. There have been no reports describing how a volatile anaesthetic affects haemodynamic responses, seizure duration, and recovery characteristics during electroconvulsive therapy. We carried out a repeated-measure crossover study to compare the effects on haemodynamic responses, seizure duration, and recovery characteristics of the following types of anaesthesia in electroconvulsive therapy: propofol alone, sevoflurane alone, and propofol combined with sevoflurane.We recruited 50 patients requiring electroconvulsive therapy for depression. For anaesthesia induction, 1.5 mg/kg propofol (condition P), 5% sevoflurane in oxygen following a vital capacity rapid inhalation induction (condition S), or 1.5 mg/kg propofol followed by 5% sevoflurane in oxygen (condition PS) was administered. Succinylcholine 1.5 mg/kg was then given. Electrical stimulation was administered after fasciculation. Measurements were obtained before anaesthesia induction (baseline), prior to succinylcholine administration, prior to electroconvulsive therapy, and at the peak after electroconvulsive therapy.After electroconvulsive therapy, peak heart rate and peak mean arterial pressure were highest in condition S. Whereas recovery time was longest in condition PS, motor seizure duration was significantly shorter than in either condition P or S. Electroencephalographic seizure duration was significantly shorter in condition PS than in condition P and significantly shorter in condition S than in condition P.Sevoflurane anaesthesia alone is most disadvantageous in terms of haemodynamics. Propofol-sevoflurane anaesthesia is advantageous in terms of haemodynamics, but disadvantageous in terms of seizure duration and recovery time. Propofol alone is most advantageous in terms of seizure duration.

Electroconvulsive therapy (ECT) is commonly associated with acute hyperdynamic cardiovascular responses, and we hypothesize that intravenous lignocaine can blunt this response. We have measured the effect of lignocaine 1.5 mg/kg IV on heart rate and mean arterial pressure during electroconvulsive therapy. Furthermore, we also assessed seizure duration using both the cuff method and two-lead electroencephalography.We studied 25 patients using a randomized, double-blind, placebo-controlled crossover study design. Patients in the control group were given intravenous saline 0.075 ml/kg, and those in the lignocaine group were given intravenous lignocaine 2% 1.5 mg/kg, and this treatment was conducted one minute before intravenous propofol 1.5 mg/kg to induce unconsciousness. Succinylcholine 1.5 mg/kg was then administered intravenously and electrical stimulation was administered after fasciculation. Measurements were taken at the baseline, prior to succinycholine, prior to electroconvulsive therapy and at the peak response after electroconvulsive therapy.Intravenous lignocaine significantly reduced the increases in heart rate after electroconvulsive therapy, as compared with the placebo. The use of intravenous lignocaine was, however, associated with a remarkably shortened seizure duration.Due to the reduction in seizure duration, routine administration of intravenous lignocaine may not be advisable since it may interfere with the psychotherapeutic efficacy of electroconvulsive therapy. However, intravenous lignocaine medication for electroconvulsive therapy is potentially useful for reducing tachycardia in high-risk patients and reducing the severity of propofol injection pain in comparison with a placebo.

In a randomized, double-blind, controlled study, we have compared two groups of patients receiving either continuous systemic i.v. or continuous brachial plexus infusion of butorphanol for analgesia after operations on the upper extremities. Twenty-two patients undergoing elective upper extremity surgery were allocated randomly to one of two groups to receive either butorphanol i.v. and saline injected into the brachial plexus sheath (i.v. group) or butorphanol injected into the brachial plexus sheath and saline i.v. (brachial plexus group). After surgery on the upper extremity under continuous axillary brachial plexus block, each patient received a continuous infusion of butorphanol either i.v. or into the brachial plexus sheath at a dose of 83.3 micrograms h-1. Concurrently, a saline infusion was given via the alternate route. Patients rated their pain on a 10-cm visual analogue scale (VAS). VAS scores in the two groups did not differ up to 6 h and 24 h after operation. From 9 h until 24 h after operation, pain scores were significantly higher in the i.v. group than in the brachial plexus group. The VAS score 9 h after operation was 3.3 (SD 2.7) in the i.v. group and 0.6 (0.9) in the brachial plexus group (P < 0.01); 12 h after operation 2.7 (1.8) in the i.v. group and 0.6 (0.9) in the brachial plexus group (P < 0.01); 18 h after operation 1.7 (1.0) in the i.v. group and 0.7 (1.0) in the brachial plexus group (P < 0.05); and 24 h after operation 3.2 (2.4) in the i.v. group and 0.7 (1.2) in the brachial plexus group (P < 0.01). We conclude that continuous injection of butorphanol into the brachial plexus sheath provided superior analgesia compared with continuous i.v. injection.

We examined the analgesic effects of orally administered clonidine on pain induced by injection of propofol (Diprivan; 2,6-diisopropyl phenol). Female patients (n=81) were randomly allocated to one of two groups: oral clonidine (5.5 microg kg(-1)) followed by i.v. propofol and a control group given placebo followed by i.v. propofol. The median pain score in the group receiving clonidine, using a four-point scale (0=no pain, 1=minimal pain, 2=moderate pain, 3=severe pain) was 1 (0-2), significantly lower than in the control group [2 (1-3), median (25-75 percentiles), P<0.001].

Nizatidine, a new H2-receptor antagonist, has been reported to inhibit acetylcholinesterase activity. This could lead to an interaction with neuromuscular blocking drugs. This study examined the effects of nizatidine on the actions of vecuronium. Oral nizatidine has been reported to be an effective protective agent against acid aspiration syndrome, and we reevaluated this effect.The control group (n=10) received a placebo with water 50 ml and the nizatidine group (n=10) received nizatidine 300 mg with water 50 ml two hours before arrival in the operating room. Gastric contents were aspirated and the volume and pH measured before induction of anaesthesia. Anaesthesia was induced in all patients with thiopentone 5 mg/kg and 1.5% isoflurane in 98.5% oxygen followed by vecuronium 0.1 mg/kg. Vecuronium onset time and duration time 25 (time from injection until recovery of 25% of vaseline twitch amplitude) were obtained using electromyography.There were no significant differences between the two groups in vecuronium onset time or duration time 25. Gastric fluid volume was greater and gastric pH was lower in the control group than in the nizatidine group. 70% of the control group and none of the nizatidine group (P<0.005) had a gastric content pH <2.5 or volume >25 ml.

Background. Lung resistance increases after induction of anaesthesia. We hypothesized that prophylactic bronchodilation with i.v. carperitide before tracheal intubation would decrease airway resistance and increase lung compliance after placement of the tracheal tube in both smokers and nonsmokers. Methods. Ninety-seven adults aged between 24 and 59 yr were randomized to receive i.v. normal saline (0.9% saline) (control) or carperitide, 0.2 µg kg−1 min−1 throughout the study. The 97 patients included smokers and nonsmokers. Thus the patients were allocated to one of the four groups: smokers who received normal saline (n=21), nonsmokers who received normal saline (n=27), smokers who received carperitide (n=19) or nonsmokers who received carperitide (n=30). Thirty minutes after starting normal saline or carperitide infusion, we administered thiamylal 5 mg kg−1 and fentanyl 5 µg kg−1 to induce general anaesthesia and vecuronium 0.3 mg kg−1 for muscle relaxation. Continuous infusion of thiamylal 15 mg kg−1 h−1 followed anaesthetic induction. Mean airway resistance (Rawm), expiratory airway resistance (Rawe) and dynamic lung compliance (Cdyn) were determined 4, 8, 12 and 16 min after tracheal intubation and compared between the four groups. Results. At 4 min after intubation, Rawm and Rawe were higher and Cdyn lower in smokers than in nonsmokers in the control group. Rawm and Rawe were lower and Cdyn higher in smokers in the carperitide group than in smokers in the control group. Rawm and Rawe were lower in nonsmokers in the carperitide group than in nonsmokers in the control group. Conclusions. Marked bronchoconstriction occurred in the control groups (smokers and nonsmokers) 4 min after tracheal intubation. Prophylactic treatment with carperitide before induction of anaesthesia and tracheal intubation was advantageous, particularly in smokers.