The neuromuscular blocking effect of vecuronium on the human diaphragm

This study compares the neuromuscular blocking effect of vecuronium (0.1 mg/kg) on the diaphragm and the adductor pollicis in nine anesthetized patients. Monitoring of the diaphragm consisted of measurement of the transdiaphragmatic pressure after bilateral phrenic nerve stimulation. Onset time for neuromuscular blockade of the diaphragm was 1.6 +/- 0.3 min (+/-SD) compared to 2.5 +/- 0.3 min in the adductor pollicis (P less than 0.001). The diaphragm recovered earlier and more rapidly than the adductor pollicis. The twitch height (TH) returned to 25% of its control value after 27 +/- 8 min for the diaphragm, compared to 41 +/- 11 min for the adductor pollicis (P less than 0.01). Complete TH recovery was achieved after 49 +/- 14 min for the diaphragm and after 74 +/- 22 min for the adductor pollicis (P less than 0.01). The recovery index of 12 +/- 4 min for the diaphragm was significantly shorter (P less than 0.05) than for the adductor pollicis (20 +/- 9 min.) We conclude that monitoring of peripheral muscles in anesthetized patients given vecuronium provides adequate information about the degree of paralysis of the diaphragm.     

The ulinastatin-induced effect on neuromuscular block caused by vecuronium

We examined the effect of ulinastatin, a protease inhibitor purified from human urine, on neuromuscular block caused by vecuronium. Sixty adult patients were randomly divided into four groups of 15 patients each: ulinastatin-posttetanic count (U-PTC), ulinastatin-train-of-four (U-TOF), control-posttetanic count (C-PTC) or control-train-of-four (C-TOF) group. In the U-PTC and U-TOF groups, a bolus dose of ulinastatin 5000 U/kg was administered 2 min before the injection of vecuronium 0.1 mg/kg. In the C-PTC and C-TOF groups, normal saline was administered instead of ulinastatin. The onset of neuromuscular block in the U-PTC and U-TOF groups was significantly slower than in the C-PTC and C-TOF groups (250+/-49 vs 214+/-35 s, mean +/- SD, P < 0.05). The time from the vecuronium injection to the return of PTC in the U-PTC group was significantly shorter than in the C-PTC group (11.0+/-2.8 vs 17.6+/-6.8 min, P < 0.05). Similarly, times to the returns of T1, T2, T3, and T4 (first, second, third, and fourth stimulation of TOF) in the U-TOF group were significantly shorter than in the C-TOF group (18.5+/-5.0 vs 28.0+/-9.1 min for T1, P < 0.05). PTC in the U-PTC group was significantly higher than in the C-PTC Group 10-30 min after the administration of vecuronium (P < 0.05). T1/control twitch height and TOF ratios in the U-TOF group were significantly higher than those in the C-TOF Group 30-70 min and 40-70 min after the administration of vecuronium, respectively (P < 0.05). Ulinastatin delays the onset of neuromuscular block and hastens its recovery caused by vecuronium. IMPLICATIONS: Ulinastatin delays the onset of neuromuscular block and hastens its recovery caused by vecuronium. This is because ulinastatin may release acetylcholine at the neuromuscular junction and increase hepatic and/or renal clearance of vecuronium.     

Onset and duration of neuromuscular blockade following high-dose vecuronium administration

To determine the onset time and duration of high doses of vecuronium, 40 ASA Physical Status 1 and 2 patients were randomly assigned to receive either 100, 200, 300, or 400 micrograms/kg of vecuronium bromide for muscle relaxation during elective general surgery. Neuromuscular blockade was continuously quantitated by recording the electromyographic response to stimulation of the ulnar nerve train-of-four. The rate of onset of neuromuscular blockade, endotracheal intubating conditions, duration of neuromuscular blockade, and hemodynamic effects of vecuronium at each dose were evaluated and compared. The time from vecuronium administration to complete abolition of twitch tension (T1 = 0%) decreased from 208 +/- 41 to 106 +/- 35 s as the vecuronium dose was increased from 100 to 400 micrograms/kg (P less than 0.01). Corresponding times to endotracheal intubation (T1 less than 20%) also decreased from 183 +/- 24 to 96 +/- 31 s with increasing doses (P less than 0.01). Recovery time (T1 = 25%) increased from 37 +/- 13 to 138 +/- 24 min with increasing doses (P less than 0.01). No significant hemodynamic differences between the four groups were observed. Endotracheal intubating conditions were good or excellent in all patients. High doses of vecuronium may, therefore, be a useful alternative to succinylcholine when a rapid onset of neuromuscular blockade is required.     

Sevoflurane exposure time and the neuromuscular blocking effect of vecuronium

Purpose  To determine the effect of sevoflurane exposure time on the duration of vecuronium neuromuscular blockade. Methods  In 40 adult patients anesthesia was induced with 1.5–2 mg·kg⁻¹ propofol and 3–5 μg·kg⁻¹ fentanyl and the trachea was intubated without the aid of muscle relaxant. Patients were randomized into four groups of 10. In group 1, 0.05 mg·kg⁻¹ vecuronium was administered with N₂O and anesthesia was maintained by propofol infusion and fentanyl. Vecuronium was administered with sevoflurane 2% in 30 patients, commencing at the same time (group 2) and at 30, and 60 min after sevoflurane (groups 3, 4). Adductor pollicis force of contraction to train-of-four ulnar nerve stimulation was recorded. Times from vecuronium injection to 95%, maximal block, and recovery times to 25% recovery were recorded. Results  There were no differences in times to 95% and maximal block in the four groups. Recovery times were longer in groups 3 and 4 than in groups 2 and 1 (P < 0.01). Times to 5% recovery were 15.0 ± 3.7, 17.8 ± 4.8, 28.2 ± 9.9, and 29.5 ± 9.5, and to 25% recovery were 22.3 ± 5.2, 27.2 ± 6.4, 42.3 ± 16.3, and 50.5 ± 16.4 in groups 1, 2, 3, and 4 respectively. No differences were found between group 1 and group 2 nor between group 3 and group 4. Conclusion  Sevoflurane produced time-dependent potentiation of vecuronium. After 30 min exposure, 25% recovery was prolonged by 89% and after 60 min by more than 100% compared with the control group. Objectif  Déterminer l’effet du temps d’exposition au sévoflurane sur la durée du blocage neuromusculaire avec du vécuronium. Méthode  On a induit l’anesthésie avec 1,5–2 mg·kg⁻¹ de propofol et 3–5 μg·kg⁻¹ de fentanyl chez 40 patients adultes et on a procédé à l’intubation endotrachéale sans myorelaxant. Les patients ont été répartis en quatre groupes de 10. Dans le groupe 1, on a administré 0,05 mg·kg⁻¹ de vécuronium avec N₂O et on a maintenu l’anesthésie avec une perfusion de propofol et de fentanyl. Chez 30 patients, le vécuronium a été administré avec le sévoflurane 2 %, en même temps aux patients du groupe 2, mais 30 et 60 min après le sévoflurane à ceux des groupes 3 et 4. La force de contraction de l’adducteur du pouce à la stimulation en train-de-quatre du nerf cubital a été notée. Le temps nécessaire pour que le vécuronium injecté produise 95 % du bloc, puis le bloc maximal, et le temps nécessaire pour atteindre une récupération de 25 %, ont été enregistrés. Résultats  II n’y a pas eu de différence de temps intergroupe pour produire 95 % du bloc, ni pour le bloc maximal. La récupération s’est prolongée dans les groupes 3 et 4 comparés aux groupes 2 et 1 (P < 0,01). Le temps nécessaire pour atteindre une récupération de 5 % ont été de 15,0 ± 3,7, 17,8 ± 4,8, 28,2 ± 9,9, et de 29,5 ± 9,5, et pour une récupération de 25 % ont été de 22,3 ± 5,2, 27,2 ± 6,4, 42,3 ± 16,3, et de 50,5 ± 16,4 dans les groupes 1, 2, 3, et 4 respectivement. Aucune différence n’a été rapportée entre les groupes 1 et 2, ni entre les groupes 3 et 4. Conclusion  Le sévoflurane a produit une potentialisation du vécuronium dépendante du temps. Après 30 min d’exposition le temps nécessaire pour produire une récupération de 25 % s’est accru de 89 % et, après 60 min, de plus de 100 %, si on le compare au temps du groupe témoin.     

Early neuromuscular recovery characteristics following administration of mivacurium plus vecuronium

Purpose

This study was designed to describe the early recovery characteristics, as well as the speed of onset of neuromuscular block, after a combination of mivacurium and vecuronium.

Methods

In this controlled, randomized study, 30 consenting ASA I–III patients were assigned to three treatment groups. The “2M2V” group received twice the dose necessary to cause 95% depression of the evoked twitch response (2 × ED₉₅) of mivacurium (0.15 mg · kg^?1) plus 2 × ED₉₅ of vecuronium (0.1 mg · kg^?1); the “2V” group received 2 × ED₉₅ of vecuronium; and the “4V” group received 4 × ED₉₅ of vecuronium. Evoked neuromuscular responses of the adductor pollicis were assessed with an adductor pollicis force transducer. The time until maximum block and times to 10% and 25% recovery (T₁₀ and T₂₅) in each group were expressed as mean ± standard deviation and compared using ANOVA.

Results

Onset of block in the 2M2V group was 27% faster than in the 2V group (2.0 ± 0.6 vs. 2.7 ± 0.8 min respectively, P < 0.05) and was similar to the 4V group (1.95 ± 0.3 min, P = NS). The times until 10% recovery were similar in the 2M2V and 4V groups (59.9 ± 12 vs 68.2 ± 25 min, P = NS) and were slower than in the 2V group (37.2 ± 9 min, P < 0.05). Between T₁₀ and T₂₅, recovery after 2M2V resembled that after 2V (6.7 ± 3 vs 5.7 ± 1 min, P = NS) and was faster than after 4V (10.9 ± 7 min, P<0.05).

Conclusions

When 2 × ED₉₅ of mivacurium is added to 2 × ED₉₅ of an intermediate or long-acting relaxant, recovery after T₁₀ will proceed as if one had administered the longeracting agent alone.     

Unmasked residual neuromuscular block after administration of vecuronium for days

IMPLICATIONS: Significant neuromuscular block may be present in patients who have received vecuronium for days.     

Accelerated onset of vecuronium neuromuscular block with pulmonary arterial administration

The purpose of this study was to determine the onset times of vecuronium neuromuscular block administered into either the central circulation or a peripheral vein. One hundred and twenty adult patients with a pulmonary artery (PA) catheter were randomly divided into one of three groups with respect to the routes of vecuronium administration (n = 40 in each group). Anaesthesia was induced with midazolam 2.5 mg iv and fentanyl 10–50 μg · kg^{? 1} iv and maintained with intermittent doses of fentanyl 50 μg iv and nitrous oxide 60–70% in oxygen. After immobilization of the forearm in a splint, the ulnar nerve was stimulated supramaximally every 12 sec. The resulting force of the evoked thumb twitch was recorded (Myograph 2000, Biometer, Denmark). The times from the injection to the first depression of twitch response (latent onset) in patients given vecuronium 0.08 mg · kg^{? 1} into the pulmonary artery, the right atrium, and a peripheral vein on the hand were 58.0 ± 19.5, 71.5 ± 17.1, and 82.4 ± 18.0 sec (mean ± SD), respectively. The latent onset of neuromuscular block occurred sooner in patients given vecuronium into the central vein than when administered into a vein on the hand (P < 0.01). In comparing the patients given vecuronium into the central vein, the onset times to 95% twitch depression (onset) were 152.3 ± 40.7 and 168.2 ± 35.5 sec. The onset of block was found to be faster when vecuronium was administered into the pulmonary artery than into the right atrium (P < 0.01). These findings suggest that the administration of vecuronium into the pulmonary artery is one approach to accelerate neuromuscular blockade in patients with a PA catheter.     

Propofol potentiates the neuromuscular blocking effects of vecuronium in man

The possible interaction between vecuronium and propofol has been investigated in 40 healthy (ASA I-II) patients. They were randomly allocated to two groups according to the method of anesthesia; continuous propofol infusion group (propofol) and droperidol and fentanyl group (control). The electromyographic response of abductor digiti minimi was monitored at 20-s interval after train-of-four stimulations of the ulnar nerve. The ED50 and ED95 (dose required to produce a 50% and 95% depression of twitch tension, respectively,) of vecuronium in the propofol group (n = 20) were 29.4 +/- 0.5 and 56.6 +/- 2.1 micrograms.kg-1 (mean +/- SEM), and in the control group (n = 20), 36.7 +/- 1.8 and 73.6 +/- 5.2 micrograms.kg-1, respectively. Under propofol anesthesia, the cumulative dose-response curves of vecuronium were shifted to the left when compared with control ED50 and the slope showed that propofol had potentiated the action of vecuronium.     

Evolution of vecuronium requirements for stable mechanical effect: comparison with or without previous succinylcholine administration

To evaluate possible interactions between residual succinylcholine and vecuronium, the amount of vecuronium required to maintain the twitch height (TH) at 10% of its initial value was measured over a 90-min period by the on-demand infusion method in two series of 15 adult patients (ASA class I-II). One group, the vecuronium treatment (V) group, received 70 micrograms X kg-1 of vecuronium and the on-demand infusion. The second group, the succinylcholine-vecuronium treatment group (SV), was given 30 micrograms X kg-1 of vecuronium and on-demand infusion 5 min after the complete recovery of TH after administration of 1 mg X kg-1 of succinylcholine. During the first 10 min, the amount of vecuronium required to maintain TH at 10% of its control was significantly greater in the group given V than in the group given SV, 15122 +/- 856 (mean +/- SEM) vs 9851 +/- 486 micrograms X m-2 X hr-1 (P less than 0.001). Thereafter, the amount of vecuronium required to maintain TH at 10% of control was similar: 2808 +/- 275 and 3068 +/- 206 micrograms X m-2 X hr-1. When the infusion of vecuronium was stopped after 90 min, the time required for spontaneous recovery from 25 to 75% of control TH levels was similar: 20.1 +/- 3.3 min in the group given V and 18.9 +/- 2.5 min in the group given SV (not significant). We conclude that after a vecuronium on-demand infusion of long duration (lasting more than 90 min), previous succinylcholine administration does not interfere with late vecuronium requirements and the spontaneous rate of recovery of TH.     

The effect of phenytoin on the magnitude and duration of neuromuscular block following atracurium or vecuronium

Patients chronically receiving anticonvulsants have been reported to be resistant to the long-acting competitive neuromuscular blockers. This study examines the effects of atracurium and vecuronium on 100 neurosurgical patients; 50 receiving chronic phenytoin therapy (group I) and 50 controls (group II). During O2/N2O/halothane anesthesia, five patients in each group were given a bolus of vecuronium 0.1 mg/kg, and a different five patients in each group were given atracurium 0.5 mg/kg, to produce neuromuscular blockade in excess of 95%. The time to maximum blockade and the recovery from atracurium was unaffected by phenytoin therapy. Recovery from vecuronium was enhanced in the phenytoin group, as demonstrated by the recovery index, defined as the time required for recovery from 25-75% of the control neuromuscular response (7.9 +/- 2.2 min compared with 17.8 +/- 5.1 min in controls, P less than 0.005). Similarly, the total duration of neuromuscular blockade, defined as recovery to 90% of control response, was significantly shorter in the phenytoin group (31.9 +/- 6.0 min compared with 69.7 +/- 12.9 min in controls, P less than 0.001). The remaining 40 patients from each group were given a preselected dose of either vecuronium (0.02-0.06 mg/kg) or atracurium (0.10-0.25 mg/kg) during anesthesia with O2/N2O/fentanyl, to generate dose-response curves for the relaxants. Using analysis of covariance, the slopes and elevations for atracurium were found to be essentially identical in the two groups; as were the calculated ED50 and ED95. Patients receiving chronic phenytoin therapy were resistant to vecuronium-induced neuromuscular blockade. With vecuronium, the dose-response curves for the two groups were parallel; the curve for phenytoin patients was shifted to the right.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of hypercarbia and hypocarbia on pancuronium and vecuronium neuromuscular blockades in anesthetized humans

To determine the effects of hypercarbia and hypocarbia on a pancuronium or vecuronium neuromuscular blockade, 54 patients were anesthetized with halothane and 60% nitrous oxide in oxygen. In 30 patients, end-tidal PCO2 was maintained at either 25 mmHg (3.5 kPa, N = 10), 41 mmHg (5.5 kPa, N = 10), or 56 mmHg (7.5 kPa, N = 10). Five patients in each group then were given pancuronium or vecuronium 0.022 mg/kg iv. Neither maximal depressions of twitch tension nor recovery indexes (time for spontaneous recovery of twitch tension from 25 to 75% of control) were altered by hypercarbia or hypocarbia. The remaining 24 patients were divided into three equal groups. Either pancuronium (N = 8) or vecuronium (N = 8) was administered iv as continuous infusion at a rate sufficient to produce a 50% depression of twitch tension. In the remaining eight patients, no muscle relaxant was given. After twitch tension was stable, half of the patients in each group had hypercarbia induced, which depressed twitch tension in all three groups. The patients who received vecuronium had a significantly larger decrease in twitch tension than those who received pancuronium or no muscle relaxant. Conversely, in the remaining patients, hypocarbia produced a significant increase in twitch tension. There was no difference in the magnitude of the increases in twitch tension among the three groups. The authors conclude that pre-muscle relaxant administration-induced hypercarbia or hypocarbia has no effect on a subsequent neuromuscular blockade from pancuronium or vecuronium.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolongation of neuromuscular blocking effect of vecuronium by antibiotics

A case is described of prolonged neuromuscular block in a patient who was given the muscle relaxant vecuronium followed by bolus injections of the antibiotics gentamycin and clindamycin.     

The effect of neuromuscular blockade with vecuronium on hemodynamic responses to noxious stimuli in the rat

The effect of neuromuscular blockade with vecuronium on the hemodynamic responses to a noxious stimulus was investigated in male Sprague-Dawley rats. The rats were anesthetized with either halothane (group 1, n = 10), or isoflurane (group 2, n = 10). The maximum values for heart rate and mean arterial pressure during the noxious stimulus (base-tail clamp) were measured, and the maximum changes in these values (maximum minus prestimulation) were calculated. The responses were measured at two different anesthetic concentrations (0.6 X MAC, 0.75 X MAC), before and after vecuronium 1.0 mg.kg-1 iv. It was found that neuromuscular blockade with vecuronium did not reduce any of the hemodynamic responses measured, at either anesthetic concentration, in either the halothane or the isoflurane group. However, increasing the anesthetic concentration from 0.6 X MAC to 0.75 X MAC produced statistically significant (P less than 0.01) reductions in several of the responses measured. The inability of vecuronium to reduce hemodynamic responses to noxious stimuli in this study suggests that neuromuscular blockade does not alter anesthetic depth in the rat. A knowledge of this "absence of effect" may be important for investigators who need to induce muscle relaxation in laboratory animals prior to examining the effect of anesthetic agents on hemodynamic responses to noxious stimuli. The results also question the ability of neuromuscular blockade to reduce anesthetic requirement, and support the view that neuromuscular blockade does not contribute to the anesthetic state.     

The effects of sevoflurane are similar to those of isoflurane on the neuromuscular block produced by vecuronium

We have examined the interactions of 1 MAC of isoflurane andsevoflurane (and 66% nitrous oxide in oxygen) with vecuronium,using the EMG response of the abductor digiti minimi to train-of-four(TOF) stimulation of the ulnar nerve. We constructed dose-responsecurves for vecuronium in 54 patients. The curves for both isofluraneand sevoflurane had a significant leftward shift compared withthat for fentanyl-nitrous oxide anaesthesia (P < 0.01). Whenthe amplitudes of the first response (T1) had recovered to 50%of control in another 32 patients, subsequently we comparedthe spontaneous recovery rate of the ratio of the fourth tothe first TOF response (T4:T1) at 3-min intervals during the15-min period, in the presence of two volatile anaestheticsor after discontinuation of administration of anaesthetic. Therate of recovery of T4:T1 was significantly greater when bothanaesthetics were discontinued. However, this rate was similarfor both anaesthetics, suggesting that the mechanism of actionof the two anaesthetics is similar. (Br. J. Anaesth. 1994; 72:465–467)