Tactile evaluation of the response to double burst stimulation decreases, but does not eliminate, the problem of postoperative residual paralysis.

BACKGROUND: Routine perioperative monitoring with accelero-myography might prevent residual block, whereas routine tactile evaluation of the response to train-of-four (TOF) nerve stimulation does not. The purpose of this prospective, randomised and blinded study was to evaluate the effect of manual evaluation of the response to double burst stimulation (DBS3.3) upon the incidence of residual block. METHODS: Sixty adult patients scheduled for elective abdominal surgery were included in the study. Pancuronium 0.08 to 0.1 mg kg-1 was given for relaxation and tracheal intubation. For maintenance of neuromuscular block, pancuronium 1-2 mg was administered. The patients were randomly allocated into two groups. In group DBS (double burst stimulation) the degree of block during anaesthesia was assessed by manual evaluation of the response to TOF nerve stimulation. During reversal, when no fade was detectable in the TOF response, the stimulation pattern was changed to DBS3.3. The trachea was extubated when the anaesthetist judged the neuromuscular function to have recovered adequately and no fade in the DBS3.3 response could be felt. In group CC (clinical criteria) patients were managed without the use of a nerve stimulator, and the level of neuromuscular block and reversal were evaluated solely on the basis of clinical criteria. In both groups, the TOF ratio was measured by mechanomyography immediately after tracheal extubation. Also, the ability to sustain head lift for 5 s, to protrude the tongue, to open the eyes, and to lift one arm to the opposite shoulder were tested. RESULTS: The TOF ratio, as measured immediately after tracheal extubation, was significantly lower in group CC than in group DBS (means: 0.68 and 0.78, respectively), and the incidence of residual neuromuscular block defined as a TOF ratio < 0.7 was significantly higher in group CC than in group DBS (57 and 24%, respectively). The time from the first TOF measurement until the TOF ratio reached 0.8 was significantly longer in group CC than in group DBs (means: 11.5 and 6.2 min, respectively). No significant differences between the two groups of patients were found in duration of anaesthesia, in times from end of surgery to injection of neostigmine, tracheal extubation or TOF ratio 0.8, in dose of pancuronium, or in any other postoperative variable. CONCLUSION: Routine perioperative manual evaluation of the responses to TOF and DBS3.3 decreased the incidence and the degree of residual block following the use of pancuronium. It did not, however, exclude clinically significant residual paralysis, nor did it influence the amount of pancuronium used during the operation, the duration of anaesthesia or the time from end of surgery to tracheal extubation or to sufficient recovery of neuromuscular function (TOF = 0.8).

Pretreatment with pancuronium before suxamethonium administration in patients heterozygous for the usual and the atypical plasma cholinesterase gene.

The object of this study was to investigate whether pretreatment with pancuronium before i.v. injection of suxamethonium could cause prolonged neuromuscular blockade in patients heterozygous for the usual and the atypical plasma cholinesterase gene (E1uE1a). Forty-three patients, 23 with genotype E1uE1a and 20 with normal genotype (E1uE1u), were pretreated with pancuronium 0.01 mg.kg-1 followed by suxamethonium 1.5 mg.kg-1, and received either neurolept anaesthesia or halothane anaesthesia. Seven patients (E1uE1a) were given suxamethonium 1.5 mg.kg-1 without pretreatment. The duration and type of neuromuscular block were evaluated using train-of-four (TOF) nerve stimulation. Type of anaesthesia did not significantly influence the results. The duration of block following pretreatment was significantly longer in heterozygous patients than in normal patients. Time to 90% twitch height recovery was 10.7 +/- 1.2 min (mean +/- s.d.) in genotypically normal patients, and 18.0 +/- 4.2 min in patients with genotype E1uE1a. Pretreatment with pancuronium caused a significantly slower recovery of the TOF ratio (phase II block). Thus, a TOF ratio of 0.7 was always reached within 13 min in genotypically normal patients. In genotypically abnormal patients, the same TOF ratio was reached within 20 min in all but three patients. In these three patients time to 90% twitch height recovery was prolonged (18-31 min), and TOF ratio did not return to normal, but stabilized at about 0.35, 0.50, and 0.65, respectively. Injection of edrophonium restored normal neuromuscular function in 10 min. It is concluded that in patients heterozygous for the usual and the atypical gene, pretreatment with pancuronium in combination with an increased dose of suxamethonium may cause a phase II block and thus a prolonged neuromuscular block.

Does perioperative tactile evaluation of the train-of-four response influence the frequency of postoperative residual neuromuscular blockade?

The authors conducted a randomized controlled clinical trial to evaluate the usefulness of perioperative manual evaluation of the response to train-of-four (TOF) nerve stimulation. A total of 80 patients were divided into four groups of 20 each. For two groups (one given vecuronium and one pancuronium), the anesthetists assessed the degree of neuromuscular blockade during operation and during recovery from neuromuscular blockade by manual evaluation of the response to TOF nerve stimulation. In the other two groups, one of which received vecuronium and the other pancuronium, the anesthetists evaluated the degree of neuromuscular blockade solely by clinical criteria. The use of a nerve stimulator was found to have no effect on the dose of relaxant given during anesthesia, on the need for supplementary doses of anticholinesterase in the recovery room, on the time from end of surgery to end of anesthesia, or on the incidence of postoperative residual neuromuscular blockade evaluated clinically. The median (and range of) TOF ratios recorded in the recovery room were 0.75 (0.33-0.96) and 0.79 (0.10-0.97) in the vecuronium groups monitored with and without a nerve stimulator, respectively. These ratios were significantly higher than those found in the pancuronium groups, which wre 0.66 (0.06-0.90) and 0.63 (0.29-0.95), respectively. However, no difference was found between the vecuronium and pancuronium groups in the number of patients showing clinical signs of residual neuromuscular blockade, as evaluated by the 5-s head-lift test.(ABSTRACT TRUNCATED AT 250 WORDS)

Precurarization with vecuronium and pancuronium in awake, healthy volunteers: the influence on neuromuscular transmission and pulmonary function.

The influence of pretreatment with pancuronium and vecuronium on the neuromuscular transmission was compared in 24 healthy, awake, non-premedicated volunteers using train-of-four (TOF) nerve stimulation and measurement of respiratory frequency, vital capacity, inspiratory force and peak expiratory flow (PEF). The subjects were randomly allocated to one of three groups. Each subject received one dose of pancuronium and one dose of vecuronium: Group I pancuronium 0.01 mg/kg and vecuronium 0.005 mg/kg; Group II pancuronium 0.01 mg/kg and vecuronium 0.01 mg/kg and Group III pancuronium 0.01 mg/kg and vecuronium 0.015 mg/kg intravenously. The median TOF ratio decreased significantly in Groups I and II following both pancuronium and vecuronium. The TOF ratio following vecuronium in Group II was significantly lower compared to the TOF ratio following vecuronium in Group I. Only PEF decreased significantly in Group I following pancuronium and in Group II following both pancuronium and vecuronium. There was no significant difference between Group I and Group II regarding the number of subjects with signs or symptoms of partial neuromuscular blockade. Following vecuronium 0.005 mg/kg, one subject was unable to swallow and the twitch height decreased to 0.25. In Group II one subject was unable to lift her head and had difficulty in swallowing following pancuronium 0.01 mg/kg. Only four subjects entered Group III because of an unacceptably high frequency of signs and symptoms of partial neuromuscular blockade and a decrease in median TOF ratio to 0.64 following vecuronium. The subjects felt it difficult to swallow, and one subject could just sustain head lift for 10 s following vecuronium 0.015 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Dose-response curves for vecuronium during halothane and neurolept anaesthesia: single bolus versus cumulative method.

The purpose of this study was to compare the incremental, cumulative dose method and the single bolus injection technique for construction of dose-response curves for vecuronium. Dose-response curves were determined in 77 patients divided into four groups according to the anaesthetic given and the method used for construction of dose-response curves. The regression lines corresponding to the four dose-response curves were found to be parallel. For vecuronium ED50 during neurolept anaesthesia was found to be 28 micrograms kg-1 with the single bolus injection technique and 35.2 micrograms kg-1 with the incremental, cumulative dose method (P less than 0.05). During halothane anaesthesia, ED50 was found to be 25.7 micrograms kg-1 and 26.2 micrograms kg-1, respectively (P greater than 0.05). Potentiation of vecuronium by halothane was found with the cumulative method only. It is concluded that the incremental, cumulative dose method is not suitable for potency determinations of vecuronium.

Dose-response relationships and neuromuscular blocking effects of vecuronium pancuronium during ketamine anaesthesia.

The dose-response curves of vecuronium and pancuronium were compared during ketamine anaesthesia in 60 patients (ASA I). The relationship between the probit transformed depression of twitch height and the logarithm of the dose was analysed by linear regression. Vecuronium was found to be 1.2 times more potent than pancuronium. ED50 of vecuronium and pancuronium were 30.5 microgram kg-1 and 37.0 microgram kg-1, and the ED95 45.6 microgram kg-1 and 59.5 microgram kg-1, respectively. Using equipotent doses of vecuronium and pancuronium (1.6 ED95) indices of neuromuscular blockade were compared in a further 20 patients (ASA I). No statistically significant difference was found in onset time. The duration of action following vecuronium was significantly shorter than after pancuronium. The time to 25% recovery of twitch height following vecuronium 73 microgram kg-1 was 22.2 min compared with 66.6 min following pancuronium 99 microgram kg-1. Following supplementary doses of vecuronium, a statistically significant increase in duration of action was seen following the fourth and fifth doses. Reversal time of vecuronium to a train-of-four ratio of 0.7 was significantly shorter than that of pancuronium (8.3 min and 13.6 min, respectively).

Precurarization--a hazard to the patient?

Four case histories are presented illustrating the unpleasant and serious reactions that may follow precurarization with small doses of non-depolarizing muscle relaxants. The importance of preoperative information, the necessity of relating the dose of the precurarizing drug to the weight of the patient and the possibility of hypersensitivity to this drug are emphasized.

Neuromuscular blocking effects of vecuronium and pancuronium during halothane anaesthesia.

The neuromuscular blocking properties of vecuronium (Org NC 45) and pancuronium were compared in 40 patients during halothane anaesthesia. Onset time was found to be dose-dependent, but no significant difference was found between the two drugs. The duration of action of vecuronium was significantly shorter than pancuronium. Times to 90% recovery of twitch height following vecuronium 0.03 mg kg-1 and 0.057 mg kg-1 were 32.0 min and 44.9 min, respectively, compared with 72.9 min and 124.7 min following equipotent doses of pancuronium (0.042 mg kg-1 and 0.08 mg kg-1). Recovery indices following both doses of vecuronium (10.0 min and 11.8 min) were significantly shorter than after pancuronium (31.0 min and 46.9 min). The reversal times of vecuronium (times from 10% to 90% twitch height recovery) were significantly shorter than those of pancuronium (7.9 min and 7.3 min, respectively, compared with 17.1 min and 17.7 min).

Cardiac effects of vecuronium and pancuronium during halothane anaesthesia.

The cardiac effects of equipotent doses of pancuronium and vecuronium (Org NC 45) were compared in 20 patients, anaesthetized with halothane. Heart rate and arterial pressure were recorded and the systolic time intervals were evaluated from simultaneous tracings of ECG, phonocardiogram and carotid pulse curve. Pancuronium 0.08 mg kg-1 caused a significant increase in heart rate (20%), insignificant changes in arterial pressure and significant changes in systolic time intervals compatible with a minor positive inotropic action. The equipotent dose of vecuronium (0.057 mg kg-1) caused no significant changes in heart rate, arterial pressure or systolic time intervals.

Thiopentone-nitrous oxide-halothane anaesthesia and suxamethonium: pretreatment with pancuronium and gallamine.

Eighty healthy adult patients randomly allocated to four groups received pancuronium 0.01, 0.015, 0.02 mg kg-1 or gallamine 0.3 mg kg-1 i.v. 3 min before induction. Just before induction of anaesthesia, the patients were examined for signs and symptoms of neuromuscular blockade. After induction of anaesthesia with thiopentone, suxamethonium 1.5 mg kg-1 was administered i.v. Five minutes later the second dose was injected. No serious arrhythmia was seen in any of the four groups following the repeated dose of suxamethonium. However, the highest dose of pancuronium (0.02 mg kg-1) caused an unacceptably high frequency of partial neuromuscular blockade.

Halothane anaesthesia and suxamethonium I: the significance of preoperative atropine administration. A double-blind study.

Preoperative administration of atropine was evaluated during induction of halothane anaesthesia with two administrations of suxamethonium 1 mg/kg body weight, 5 min apart. Sixty-eight healthy, adult patients were studied. They were divided into five groups according to dose and route of administration of atropine. ECG was continuously monitored. Serum potassium, pH, PaCO2, PaO2 and standard bicarbonate were measured at appropriate intervals. It was found that neither atropine 0.01 mg/kg body weight given intramuscularly 1 h beofre the anaesthesia nor atropine 0.01 mg/kg body weight given intravenously 5 min prior to induction protected against serious bradycardias (defined as heart rate below 20 beats per minute) following the second dose of suxamethonium. No serious brady-arrhythmias were seen in patients given either a combination of intramuscular and intravenous atropine in the above-mentioned doses or in patients given atropine 0.015 mg/kg body weight intravenously 5 minutes prior to induction. However, a decrease in heart rate to around 40-50 beats per minute occurred in some of these patients. Furthermore, these large doses of atropine caused an increase in heart rate during induction to more than 120 beats per minute in about 50% of the patients and to more than 140 beats per minute in about 25% of the patients. Our results suggest that preoperative administration of atropine does not protect against serious brady-arrhythmias following a second dose of suxamethonium, unless doses of atropine are used which cause tachycarida of considerable degree.