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Vecuronium was used to provide muscle relaxation in a patient who subsequently developed prolonged neuromuscular blockade (8 h) after anaesthesia. The aetiology of this condition, and the possible role of vecuronium, are discussed.
The features of eight commercially available peripheral nerve stimulators were compared with those evolved as ideal for monitoring neuromuscular blockade. The pulse waveforms were satisfactory except for that delivered by the CIG series 80 nerve/muscle stimulator. The error in timing of the stimulation patterns was up to 60% in the Professional Instruments NS-2C compared with 8% or less in the other devices. All of the stimulators had maximum current outputs suitable for monitoring with surface stimulating electrodes. The current delivered by the CIG series 80 nerve/muscle stimulator and the Stimlocator SL1.4 sagged by 21% and 25% respectively during a tetanus. The Digistim III, Bard Biomedical 750 digital and the Professional Instruments NS-2C had accurate digital readouts of delivered current.
To study the effect of decreasing the concentration of enflurane on a combined enflurane-d-tubocurarine (dTC) neuromuscular blockade, six ASA class I or II patients were studied using a continuous infusion of dTC and a sequence of decreasing end-tidal concentrations of enflurane. A constant infusion of dTC and a 2.2 per cent end-tidal concentration of enflurane decreased twitch tension to 8 per cent of control. Maintaining this same infusion rate of dTC, but decreasing the end-tidal concentration of enflurane to 1.35 and 0.5 per cent, increased the twitch tension to 57 and 91 per cent of control, respectively. The authors conclude that the enflurane contribution to muscle relaxation dissipates in a dose-dependent manner as the end-tidal concentration of enflurane is reduced. This factor may provide additional safety for patients because the anesthetic produces a component of relaxation that is readily reversible with time without the use of acetylcholinesterase inhibitors.
We studied the feasibility of recording motor evoked responses to transcranial electrical stimulation (tce-MERs) during partial neuromuscular blockade (NMB). In 11 patients, compound muscle action potentials were recorded from the tibialis anterior muscle in response to transcranial electrical stimulation during various levels of vecuronium-induced NMB. The level of NMB was assessed by accelerometry of the adductor pollicis muscle after train-of-four stimulation of the ulnar nerve. The compound muscle action potential was also recorded from the tibialis anterior muscle after direct stimulation of the peroneal nerve (M-response) as an alternative means of assessing the degree of NMB. In all patients, tce-MERs could be recorded reliably during anesthesia with N2O and a continuous infusion of sufentanil (0.5 micrograms.kg-1.h-1). An intact train-of-four was present in all patients, and the amplitude of the first twitch was recorded and designated as the control value. Before administration of vecuronium, the M-response amplitude was 9.6 +/- 3.6 (mean +/- SD) mV, and the tce-MER amplitude was 1.21 +/- 0.66 mV. Although administration of vecuronium (0.05 mg/kg) resulted in loss of the mechanical adductor pollicis response in 8 of the 11 patients, the M-response and the tce-MER remained recordable. Subsequently, during an infusion of vecuronium, adjusted to maintain one or two mechanical responses to train-of-four stimulation, the average M-response to peroneal nerve stimulation was 5.2 +/- 2.5 mV (53% of the control value), and tce-MER amplitude was 0.59 +/- 0.36 mV (59% of the control value).(ABSTRACT TRUNCATED AT 250 WORDS)
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PURPOSE: Phonomyography (PMG) is a novel technique for measuring neuromuscular blockade (NMB). The effect of the duration of control stimulation on the onset and duration of blockade was investigated using PMG and acceleromyography (AMG). METHODS: After induction of anesthesia, a microphone was placed above the middle portion of the left eyebrow, and an acceleromyographic probe was placed above the middle portion of the right eyebrow. Twenty patients were randomized to receive bilateral, single-twitch, facial nerve stimulation (0.1 Hz, 20 mA) with three minutes (n = 10) or ten minutes (n = 10) of supramaximal stimulation before mivacurium 0.2 mg.kg(-1) was administered. Onset, maximum effect, and offset of NMB were measured. RESULTS: Using PMG, lag time, onset time, maximum effect, and time to reach 75% of control twitch height (mean +/- SD) were 36 +/- 27 sec, 136 +/- 35 sec, 89 +/- 10%, and 12.1 +/- 4.5 min, respectively, after three minutes of control stimulation and were 40 +/- 22 sec, 122 +/- 40 sec, 93 +/- 3%, and 12.4 +/- 4.9 min, after ten minutes. Using AMG, the values were 38 +/- 23 sec, 106 +/- 28 sec, 79 +/- 6%, and 14.3 +/- 5.9 min, respectively, after three minutes and were 34 +/- 22 sec, 106 +/- 28 sec, 76 +/- 10%, and 14.9 +/- 3.7 min, after ten minutes. Compared to PMG, AMG revealed significant bias for onset time (-30 sec), maximum effect (-16%) and time to reach 75% of control twitch height (1.5 min), with wide limits of agreement of 66 sec, 22%, and 5.6 min, respectively. CONCLUSION: The duration of control stimulation did not influence the time course of blockade measured by either method. Three minutes of supramaximal stimulation is sufficient to measure pharmacodynamic parameters. AMG measures a shorter onset and longer recovery time and reduced anesthesiology the maximum effect compared to PMG.
A new stimulator is described with characteristics designed to take advantage of recent knowledge of the pharmacology of neuromuscular relaxants and events involved in normal neuromuscular transmission. The stimulator has proven as useful in performance of peripheral nerve blocks as in monitoring neuromuscular blockade.
This study determined the characteristics of the neuromuscular block which followed intramuscular succinylcholine 4 mg . kg-1 in 20 infants during halothane anaesthesia. The infants were divided into two groups of ten; the first received succinylcholine in two percent solution and the second in five per cent solution. The mean maximum depression of the first twitch of the train-of-four (T1) was 89.7 +/- 5.0 per cent in 4.0 +/- 0.6 min, and the mean full recovery of T1 occurred in 15.6 +/- 0.9 min after injection. The maximum block achieved and the onset and recovery times were not affected by the concentration used. Depolarizing block, with equal depression of all twitches of the train-of-four was observed during the onset of neuromuscular blockade. During recovery, phase II block, as determined by a train-of-four ratio (T4/T1) of 0.5 or less, occurred frequently at T1 recovery of 25-50 per cent, but was not associated with prolonged paralysis. It is concluded that the onset time of 4 min for intramuscular succinylcholine 4 mg . kg-1 may be too long for emergency use in infants, and no improvement is obtained by increasing the concentration of injected succinylcholine from two to five per cent.
The characteristics of the train-of-four (TOF) response were studied electromyographically during onset and spontaneous offset of neuromuscular blockade with bolus doses of vecuronium (ED95, and ED95 X 2). During onset of blockade there was less fade with the larger than the smaller dose of vecuronium, demonstrating a variable and dose-related relationship between the ratio of height of the initial twitch, T1, and fourth twitch, T4. With both doses TOF fade was more pronounced during recovery than during onset of block, but at the same T1 values during offset, both doses were associated with similar degrees of fade during recovery. Thus with bolus doses of vecuronium the T4 ratio during recovery bears a fixed relationship to initial T1 depression that is independent of dose.
Impaired parasympathetic control of heart rate is associated with increased incidence of cardiac dysrhythmias and ischemia. Anticholinergic drugs suppress parasympathetic control and could be detrimental in the early postoperative period in high-risk patients. In this double-blind randomized trial, 30 ASA physical status I and II patients undergoing minor surgery received either atropine 20 micrograms/kg and neostigmine 50 micrograms/kg (Group A), glycopyrrolate 8 micrograms/kg and neostigmine 50 micrograms/kg (Group G), or placebo (Group P) for reversal of neuromuscular blockade. Two indices of parasympathetic modulation of heart rate, spontaneous baroreflex sensitivity, and high-frequency heart rate variability, were assessed. At 2 h after reversal, Group A showed persisting impairment of baroreflex sensitivity with respect to Group P (7.12 +/- 0.86 vs 12.71 +/- 1.38 ms/mm Hg, P = 0.022) as well as decreased high-frequency heart rate variability (280.8 +/- 30.1 vs 569.2 +/- 115.2 ms2/Hz, P = 0.015). Groups A and G showed a borderline decrease in normalized high-frequency variability at 2 h (P = 0.05 for Groups A and G versus Group P). Anticholinergic drugs with neostigmine cause impairment of parasympathetic control of heart rate which persists into the early postoperative period. The effects of glycopyrrolate appear to be of shorter duration; this drug may thus be preferable in patients at risk of cardiovascular complications.
OBJECTIVE: The objective of this study was to determine whether changes in nondepolarizing neuromuscular blockade (NMB) alter the latency or amplitude of visual, brain stem auditory, or median nerve somatosensory evoked potentials. METHODS: Ten adult cynomologous Macaca fascicularis monkeys were studied during continuous ketamine anesthesia infusion. The NMB was incrementally adjusted between no block and complete block using infusions of vecuronium or atracurium. The NMB was measured by observing the mechanical response of the hand muscles to train-of-four stimulation of the median nerve and by quantification of the peak-to-peak electromyographic activity of the thenar muscles to supramaximal median nerve stimulation. The following variables were measured: the latencies of the three major peaks of the brain stem auditory evoked potential, the latency and amplitude of the cortical visual evoked potential, the latency of the spinal cord response, and the latency and amplitude of the cortical median nerve somatosensory evoked response. RESULTS: No statistically significant changes were observed for any evoked response variable measured at any degree of NMB when compared with values obtained in the unblocked control state. CONCLUSIONS: The results suggest that fluctuating degrees of NMB may contribute little to changes in these evoked potentials during intraoperative monitoring, given the testing parameters used.
Intramuscular injection of botulinum toxin A is used to treat focal dystonias. Because immunoresistance has been documented in some patients, other molecular forms of the toxin have been evaluated clinically. The present investigation compared the time course and extent of neuromuscular blockade and recovery of botulinum toxin types A and F using an electromyographic monitoring system implanted in the rat hindlimb. For a given dose, the degree and duration of blockade was more complete with type A toxin. Delayed onset of recovery in animals that received high doses of type A toxin allowed time for denervative changes to prevent a full return to baseline, as confirmed histologically. Conversely, animals receiving type F toxin fully recovered within 30 days at all dose levels. The rapid recovery with type F toxin suggested that neuromuscular transmission was restored via the original terminals rather than through functional collateral sprouting. The reversible nature of blockade with this molecular species puts in question its future clinical utility.
OBJECTIVE: To investigate in vitro effects of isoeugenol on neuromuscular transmission in tissues obtained from rats. SAMPLE POPULATION: Tissues (phrenic nerve and diaphragm) obtained from 15 male Sprague-Dawley rats. PROCEDURE: Rats were euthanatized, and tissues (phrenic nerves and diaphragm) were obtained. Phrenic nerve-diaphragm preparations were examined in vitro. The phrenic nerve was stimulated with weak electrical impulses. Muscle-twitch responses were recorded before and after the addition of drugs (pancuronium, neostigmine, isoeugenol, and benzocaine). RESULTS: Pancuronium and isoeugenol in low concentrations (10 to 206 microM) caused a distinct decrease in twitch response, which could be reversed by the addition of neostigmine. The decrease in twitch response caused by benzocaine or high concentrations of isoeugenol could not be reversed by the addition of neostigmine. CONCLUSIONS AND CLINICAL RELEVANCE: Isoeugenol caused a competitive blockade of neuromuscular transmission. Neostigmine restored this transmission by inhibiting acetylcholinesterase, which led to increased concentrations of acetylcholine. Because isoeugenol is used as an anesthetic in fish, further investigations are necessary to determine whether fish exposed to isoeugenol are sedated and unconscious or whether they are only paralyzed but have intact perception in afferent sensory nerves.
The authors sought to determine whether the metabolites of neostigmine and pyridostigmine contribute to antagonism of neuromuscular blockade. Accordingly, the dose-response relationship, onset and duration of action (n = 60), and pharmacokinetics (n = 22) of neostigmine, pyridostigmine, their metabolites 3-hydroxyphenyltrimethylammonium (PTMA) and 3-hydroxy-N-methylpyridinium (MP), and edrophonium were determined in dogs anesthetized with sodium pentobarbital. The force of contraction of the anterior tibialis muscle was maintained at constant 90% depression by infusing pancuronium. Then, a single iv bolus dose of one of the drugs under study was injected while the pancuronium infusion was continued. Venous blood, urine, and bile were sampled for four hours. Concentrations were determined by liquid chromatographic techniques; a three-compartment pharmacokinetic model was fitted to the serum concentration data. The doses producing 50% antagonism were 6.5, 52, 69, and 40 micrograms/kg for neostigmine, pyridostigmine, edrophonium, and PTMA, respectively. MP was inactive as an antagonist. By comparing approximately equipotent doses, time to peak antagonism (onset) and until 30% of peak antagonism remained (duration) were shorter for both edrophonium and PTMA than for neostigmine and pyridostigmine. Slow distribution and elimination half-lives, volume of distribution at steady state (VDss), and total plasma clearance (Cl) were similar for the drugs except for a smaller Vdss and lower Cl for MP. More than 60% of the dose of each drug was recovered unchanged from urine; less than 1% was recovered from bile. Less than 10% of the dose of neostigmine was recovered as PTMA.(ABSTRACT TRUNCATED AT 250 WORDS)
This is a case report with postoperatively prolonged neuromuscular blockade of 17 hours duration suspected to be caused by trimetaphan. Inhibitory action of trimetaphan to true cholinesterase (human red cell cholinesterase) was estimated in vitro, and it is concluded that this action is too weak to cause neuromuscular disturbances by acetylcholine excess in clinical doses. Trimetaphan is considered to have a neuromuscular blocking action of a non-depolarising type.
A patient with unrecognized atypical pseudocholinesterase was given succinylcholine and then vecuronium before neuromuscular monitoring was instituted. Subsequently, when neostigmine and glycopyrrolate were given to reverse what was thought to be a nondepolarizing block, the patient became further relaxed, and his trachea could not be extubated for more than 10 hours. In this report, we discuss drug interactions, phase II block, and the importance of timely neuromuscular monitoring.
The purpose of this study was to develop a simple and noninvasive method for the quantitative evaluation of neuromuscular blockade in mice. The sciatic nerve in anesthetized animals (etomidate, 50 mg/kg or mephenesin, 250 mg/kg) was stimulated using transcutaneous electrodes; repetitive supramaximal stimulations (3 Hz during 3.3 sec) were applied each minute until recovery or death occurred. Evoked action potentials of the gastrocnemius muscle were recorded. The effect of each pharmacological agent was expressed as the ratio (S5/S1) of the area of the fifth response (S5) to the first one (S1). The performance of the method was tested using neuromuscular blocking agents such as alcuronium, suxamethonium, or alpha-bungarotoxin. It was concluded that the method exhibits the required statistical performances (sensitivity, repeatability, and specificity) to be recommended for in vivo investigation of neuromuscular impairment.
The present study was undertaken to determine the site of action of trimethaphan in causing neuromuscular blockade using isolated rat and frog muscle. Trimethaphan and d-tubocurarine attenuated the twitch tension developed by nerve stimulation, trimethaphan being 1/100 to 1/200 as potent as d-tubocurarine. Neostigmine potentiated the inhibitory effect of trimethaphan but reversed the effect of d-tubocurarine. Trimethaphan shifted the dose response curve of frog rectus abdominis muscle for carbachol downwards, while d-tubocurarine shifted the curve parallel to the right. Treatment with d-tubocurarine or succinylcholine protected acetylcholine receptors from persistent blockade by alpha-bungarotoxin while, in contrast, trimethaphan failed to protect the receptors. The findings indicate that trimethaphan acts on the motor endplate but, unlike d-tubocurarine, does not interact with the recognition site of acetylcholine receptors; the action of trimethaphan appears to be associated with the blockade of endplate ionic channels.