Electromyographic assessment of neuromuscular block at the gastrocnemius muscle

We have assessed neuromuscular block electromyographically at the gastrocnemius muscle and compared it with that at the abductor digiti minimi muscle in 60 adult patients undergoing cervical spine surgery under general anaesthesia. All patients were in the prone position. After vecuronium 0.2 mg kg-1, times to onset of neuromuscular block at the gastrocnemius and abductor digiti minimi muscles were mean 147 (SD 24) and 145 (14) s, respectively (ns). Times to return of the first response of the post-tetanic count (PTC1) at the gastrocnemius and abductor digiti minimi muscles were 27.7 (5.6) and 37.0 (5.9) min, respectively (P = 0.0001). Times to return of the first response of the train-of-four (TOF) at the gastrocnemius and abductor digiti minimi muscles were 41.0 (9.1) and 49.9 (8.7) min, respectively (P = 0.01). Recovery of PTC, T1/T0 and TOF ratio at the gastrocnemius muscle were significantly faster than at the abductor digiti minimi muscle.      

Magnesium sulphate enhances residual neuromuscular block induced by vecuronium

Magnesium sulphate (MgSO4) is currently used for haemodynamic control during anaesthesia and the early postoperative period. We have investigated the effect of this treatment on residual neuromuscular block after administration of vecuronium. Twenty adult patients were allocated randomly to one of two groups to receive MgSO4 60 mg kg-1 either at recovery from vecuronium block to a train-of-four (TOF) ratio of 0.7, or 1 h after recovery to a TOF ratio of 0.7. Neuromuscular transmission was monitored using electromyography and TOF stimulation. MgSO4 caused rapid and profound recurarization in all 20 patients. MgSO4 decreased the amount of acetylcholine released at the motor nerve terminal and thus may lead to recurarization in patients previously exposed to neuromuscular blocking agents.      

Antagonism of vecuronium-induced neuromuscular block in patients pretreated with magnesium sulphate: dose-effect relationship of neostigmine

We have investigated the dose-effect relationship of neostigmine in antagonizing vecuronium-induced neuromuscular block with and without magnesium sulphate (MgSO4) pretreatment. Neuromuscular block was assessed by electromyography with train-of-four (TOF) stimulation. First, we determined neostigmine-induced recovery in patients pretreated with MgSO4 (group A) or saline (group B) (n = 12 each). The height of T1, 5 min after neostigmine, was 43 (7)% in group A and 65 (6)% in group B (P < 0.01). Respective values after 10 min were 59 (7)% and 83 (5)% (P < 0.01). TOF ratio, 5 min after neostigmine, was 29 (6)% in group A and 29 (5)% in group B. Respective values after 10 min were 38 (11)% and 51 (7)% (P < 0.01). To gain insight into the mechanisms leading to delayed recovery after MgSO4, we calculated assisted recovery, defined as neostigmine-induced recovery minus mean spontaneous recovery. Spontaneous recovery was assessed in another 24 patients. Patients in group C received MgSO4/vecuronium and patients in group D vecuronium only (n = 12 each). Five minutes after neostigmine, assisted recovery was 22 (7)% in the MgSO4 pretreated patients and 28 (6)% in controls (P < 0.05). Ten minutes after neostigmine, values were 24 (7)% and 22 (6)%. Maximum assisted recovery was not influenced by MgSO4 pretreatment (27 (6)% in group A and 32 (6)% in group B) and time to maximum effect was comparable between groups: 6 (4-10) min and 7 (5- 8) min, respectively. We conclude that neostigmine-induced recovery was attenuated in patients treated with MgSO4. This was mainly a result of slower spontaneous recovery and not decreased response to neostigmine.      

Interaction of magnesium sulphate with vecuronium-induced neuromuscular blockt

We have investigated the interaction between magnesium sulphate40 mg kg^–1 i.v. and vecuronium. First, we determined theeffect of pretreatment with magnesium on the potency of vecuroniumusing a single bolus dose-response technique. In addition, wecompared the time course of vecuronium-induced neuromuscularblock (vecuronium 100 µg kg^–1) with and withoutmagnesium pretreatment. For both parts, neuromuscular blockwas assessed by electromyography. In addition, the effect ofmagnesium pretreatment on vecuronium-induced neuromuscular blockwas investigated in the context of rapid sequence inductionof anaesthesia. We found that the neuromuscular potency of vecuroniumwas increased by pretreatment with magnesium sul phate. TheED₅₀ and ED₉₀ of vecuronium with MgSO₄ were 25% lower than withoutMgSO₄ (ED₅₀ 21.3 vs 26.9 µg kg^–1 ED₉₀ 34.2 vs 45.7µg kg^–1 P < 0.05 for both). Mean onset time was147.3 (SD 22.2) s in the MgSO₄ group vs 297.3 (122) s for controls(P < 0.05). Clinical duration was prolonged (MgSO₄-vecuronium43.3 (9) min vs 25.2 (5.1) min for controls; P < 0.05). Thiswas also true for the recovery index (20.1 (6.6) mm vs 10.6(3.4) min; P < 0.05) and duration to 75% recovery (63.4 (9.9)min vs 35.8 (6.9) min; < 0.05). In the context of rapid sequenceinduction, pretreatment with MgSO₄ improved the intubating scoreof vecuronium compared with vecuronium without MgSO₄ reach ingthe same quality as that with suxamethonium 1 mg kg^–1.We conclude that magnesium pretreat ment increased the neuromuscularpotency of vecuronium, in addition to modifying the time courseof its neuromuscular block.      

Administration of magnesium sulphate before rocuronium: effects on speed of onset and duration of neuromuscular block

The speeds of onset of pancuronium, atracurium and vecuronium are increased by prior administration of magnesium sulphate. A prospective, randomized, double-blind, controlled, clinical study was performed to examine the effects of prior i.v. administration of magnesium sulphate 60 mg kg-1 on the neuromuscular blocking effects of rocuronium 0.6 mg kg-1 during isoflurane anaesthesia. Neuromuscular function was measured electromyographically (Relaxograph) in 30 patients who received either magnesium sulphate 60 mg kg-1 or normal saline, 1-min before rocuronium 0.6 mg kg-1. Mean onset times were similar in the two groups (magnesium sulphate 71 (SD 20) s; normal saline 75 (23) s), but times to initial, 10% and 25% recovery from neuromuscular block were significantly longer in the magnesium sulphate group (42.1 (16.3), 49.0 (12.4) and 56.5 (13.2) min, respectively) than in the saline group (25.1 (9.1), 33.0 (11.1) and 35.6 (13.2) min, respectively) (P < 0.05 in all three cases). Administration of magnesium sulphate was not associated with adverse haemodynamic effects. Prior administration of magnesium sulphate, under the study conditions described, prolonged rocuronium- induced neuromuscular block but did not increase speed of onset.      

Time course of rocuronium‐induced neuromuscular block after pre‐treatment with magnesium sulphate: a randomised study

Background: A previously published study suggested that pre‐treatment with magnesium sulphate (MgSO₄) had no impact on the speed of onset of rocuronium‐induced neuromuscular block. We set out to verify this assumption. Methods: Eighty patients (18–60 years) were randomly allocated to MgSO₄ 60 mg/kg or placebo (saline). Study drugs were given intravenously for 15 min before induction of anaesthesia with propofol, sufentanil and rocuronium 0.6 mg/kg. Anaesthesia was maintained with a target‐controlled propofol infusion. Neuromuscular transmission was measured using train‐of‐four (TOF)‐Watch SX^® acceleromyography. Results: Onset was analysed in 37 MgSO₄ and 38 saline patients, and recovery in 35 MgSO₄ and 37 saline patients. Onset time (to 95% depression of T1) was on average 77 [SD=18] s with MgSO₄ and 120 [48] s with saline (P<0.001). The total recovery time (DurTOF0.9) was on average 73.2 [22] min with MgSO₄ and 57.8 [14.2] min with saline (P<0.003). The clinical duration (Dur25%) was on average 44.7 [14] min with MgSO₄ and 33.2 [8.1] min with saline (P<0.0002). The recovery index (Dur25–75%) was on average 14.0 [6] min with MgSO₄ and 11.2 [5.2] min with saline (P<0.02). The recovery time (Dur25%TOF0.9) was on average 28.5 [11.7] min with MgSO₄ and 24.7 [8.4] min with saline (P=0.28). Conclusion: Magnesium sulphate given 15 min before propofol anaesthesia reduces the onset time of rocuronium by about 35% and prolongs the total recovery time by about 25%. Trial Registration: Clinicaltrials.gov identifier: NCT00405977.     

Some characteristics of neuromuscular block in the respiratory musculature in anaesthetized man.

The ability to breathe against a mild expiratory obstruction was examined in 64 adult patients under halothane-nitrous oxide-oxygen anaesthesia. The trachea of all patients were incubated. It was found that d-tubocurarine 0.11 mg/kg blocked the respiratory musculature by 50 per cent. The onset of block was immediate, with the peak effect reached within one minute. The duration of block was either very short (1 to 2 minutes) or long (paralleling the blockade in the thumb twitch), depending upon the dose of d-tubocurarine. Following injection of a small dose (up to 0.1 mg/kg) the respiratory musculature might be blocked by 30 per cent but for only one minute, disproportionately short as compared with the thumb twitch. Following injection of a large dose (0.1-0.3 mg/kg) the duration was long, but the recovery was only slightly ahead of the thumb. Following an intermediate dose, a biaphasic pattern was observed. An initial partial recovery was observed during the first 1 to 2 minutes. Comparison of the respiratory musculature and the thumb twitch revealed that the respiratory musculature was highly sensitive to block and has a different time course. Succinylcholine 0.08 mg/kg blocked the respiratory force by 50 per cent with a time course similar to the block in the thumb twitch. The clinical significance of these observations are discussed.     

Atropine sulphate enhances neuromuscular transmission in the rat

The effect of atropine (0.001-10 mumol.l-1) on neuromuscular transmission in the rat hemidiaphragm preparation was investigated by analysing its effects on directly and indirectly-elicited twitch, tetanic, post-tetanic twitch responses and on the phenomenon of post-tetanic twitch potentiation. The effect of atropine on contractions produced by endogenous acetylcholine (ACh) or exogenous ACh (added directly into organ bath containing muscle) was studied in rat ileum. The results showed that atropine in low concentrations (1 mumol.l-1 or less), enhanced the indirectly-elicited twitch, tetanic and post-tetanic twitch responses in the rat diaphragm preparation. The mean EC50 value of atropine-induced increase in twitch tension was 0.08 +/- 0.01 mumol.l-1 (mean +/- s.e. mean, n = 6). Atropine had little effect on directly-elicited twitch tension, but in high concentrations (10 mumol.l-1 or more), it reduced the directly, and indirectly-elicited twitch contractions and produced a neuromuscular block in the rat diaphragm preparation. Atropine increased the contraction produced, in rat ileum, by endogenous ACh, i.e. ACh released from the phrenic nerve stimulated at 50 Hz for 20 s duration (control contraction: 1.3 +/- 0.1 g, contraction in atropine: 1.7 +/- 0.2 g). In contrast, atropine significantly reduced the contraction produced by exogenous ACh in the same preparation (control contraction: 3.0 +/- 0.5 g, atropine: 2.0 +/- 0.1 g), suggesting that a different mechanism may be involved in the latter effect of atropine. It was concluded that atropine, in low concentration, enhanced neuromuscular transmission, possibly via a presynaptic mechanism. In high concentration, atropine may reduce and then block transmission, possibly via pre- and postsynaptic mechanisms.     

Effect of magnesium sulphate on sugammadex reversal time for neuromuscular blockade: a randomised controlled study

Magnesium potentiates neuromuscular blockade. Sugammadex reverses rocuronium‐induced blockade. The aim of this study was to determine the effect of pre‐treatment with magnesium sulphate on sugammadex reversal time for neuromuscular blockade. Seventy‐three patients were randomly assigned to receive magnesium sulphate (40 mg.kg^?1) or saline intravenously. After anaesthetic induction, continuous train‐of‐four monitoring was performed and rocuronium was administered (0.6 mg.kg^?1). When a second twitch appeared, the patients received sugammadex (2 mg.kg^?1). The median (IQR [range]) reversal time of moderate neuromuscular blockade to a train‐of‐four ratio of 0.9 facilitated by sugammadex was 115 (93?177.5 [68?315]) s in the magnesium group and 120 (105?140 [70?298]) s in the saline group (p = 0.79). The median (IQR [range]) clinical duration was 45 (35.5?53 [22?102]) min in the magnesium group and 37 (31?43 [19?73]) min in the saline group (p = 0.031). Pre‐treatment with magnesium did not significantly affect sugammadex reversal time of moderate neuromuscular blockade induced by rocuronium.     

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%.     

Antagonism of neuromuscular block in the elderly

Glycopyrronium 10 micrograms/kg has been compared with atropine 20 micrograms/kg in a mixture with neostigmine 50 micrograms/kg administered for antagonism of residual nondepolarising neuromuscular block in patients over 65 years of age. The initial peak increase in heart rate was less after glycopyrronium, but there were no differences beyond the first two minutes. The incidence of dysrhythmias was less after glycopyrronium but the difference was not significant. The control of secretions was superior with glycopyrronium. It is suggested that the dosage of anticholinergic agents given with neostigmine could be reduced in elderly patients in comparison to that in younger patients.     

Prolongation of rapacuronium neuromuscular blockade by clindamycin and magnesium.

IMPLICATIONS: We report a prolonged neuromuscular block with the nondepolarizing muscle relaxant rapacuronium in the presence of clindamycin. Even when using "short-acting" muscle relaxants, the anesthesiologist must routinely monitor the neuromuscular function.     

Reversal of neuromuscular block

The effect on heart rate of different rates of injection (10 seconds, 1, 3 and 5 minutes) of a fixed dose (neostigmine 2.5 mg and atropine 1.2 mg) and a weight-related dose (neostigmine 50 micrograms/kg and atropine 25 micrograms/kg) of neostigmine-atropine mixture given for the reversal of residual competitive neuromuscular block was studied in 196 healthy adult patients. In both series slow injection lessened and delayed the initial rise in heart rate. The subsequent fall in heart rate was less when the drugs were injected over 3 min compared with the 10 seconds and 1 minute injection groups but when given over 5 minutes there was a steady fall in heart rate, more so with the weight-related dose. It is recommended that a neostigmine and atropine mixture should be administered over 3 min.