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PubMed1989

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.

Anesthesia, Inhalation↗
PubMed1991

Neuromuscular blockade: electromyographic and mechanical versus visual interpretation.

Anesthetists frequently provide intraoperative muscle relaxation in addition to general anesthesia. However, visual interpretation of the effect of neuromuscular blocking drugs is not always possible. This study examined two alternative methods (electromyography/electrocardiography [EMG/ECG] and mechanical/ECG) of interpreting neuromuscular blockade and compared these methods to visual interpretation. EMG/ECG and mechanical/ECG methodologies were found to provide reliable valid intraoperative interpretation of nondepolarizing neuromuscular blockade for single-twitch and train-of-four stimuli. EMG/ECG and mechanical/ECG measures of neuromuscular blockade were performed with an electrocardiographic monitor and a pressure transducer, respectively. Both EMG/ECG and mechanical/ECG, when compared to visual interpretation, were found to be equally, and usually more, valid indicators of neuromuscular blockade. The clinical significance of this study is its contribution to quality care and patient safety. When visual monitoring of neuromuscular blockade is not feasible, either EMG/ECG or mechanical/ECG provide an alternative method of monitoring neuromuscular blockade.

Aged↗
PubMed1991

[Conversion to 2nd degree from 1st degree atrioventricular (AV) block by the reversal of neuromuscular blockade].

A case of intraoperative conversion to 2nd degree from 1st degree AV block by the reversal of neuromuscular blockade was reported. A 78 year old male, who originally suffered from 1st degree AV block, underwent choledocholithotomy and T-tube drainage for choledocholithiasis. He was administered 4 mg of pancuronium at the time of intubation. The operation lasted for 160 minutes under epidural anesthesia, NLA and nitrous oxide-oxygen. The patient started spontaneous breathing and the recovery was confirmed after the operation which finished without any problem. Neuromuscular blockade was reversed with atropine 0.5 mg and neostigmine 1.0 mg that were administered simultaneously taking 3 minutes. Then he was extubated without any troublesome stimulation. Suddenly, however, he suffered from the worse condition of bradycardia with the 2nd degree AV block. It took about 45 minutes until he recovered to the original 1st degree AV block despite atropine treatment. We believe that this accident was induced by a vasovagal reflex which was triggered by extubation under the effect of neostigmine which acts longer than that of atropine. We should be careful in reversing the effect of the non-depolarizing neuromuscular blockade. A short acting neuromuscular blockade, i.e. vecuronium, is preferable so as to avoid neostigmine reversal, and extubation should be performed when the effect of neuromuscular blockade is confirmed to be exhausted.

Aged↗
PubMed1997

Onset of vecuronium neuromuscular blockade at the hand with an arterio-venous shunt.

PURPOSE: To evaluate the onset of vecuronium neuromuscular blockade in the hand with an arterio-venous shunt for haemodialysis. METHODS: In 15 adult patients receiving haemodialysis for renal failure the onset of vecuronium-induced neuromuscular blockade after 0.08 mg-kg-1 vecuronium i.v. was measured. Using train-of-four mechanomyographic monitoring, the force of contraction of the adductor pollicis of both hands with and without arterio-venous shunt was measured simultaneously. RESULTS: The times from the injection to the first depression of twitch response (latent onset) and 95% twitch depression (onset) in the hand with and without arterio-venous shunt were 114.7 +/- 33.4 and 218.7 +/- 59.9 and 117.3 +/- 34.3 and 208.7 +/- 60.9 sec respectively. No difference in the onset of vecuronium neuromuscular blockade in the hand an arterio-venous shunt was demonstrated. CONCLUSION: The presence of an arteriovenous fistula does not modify the onset on neuromuscular blockade. Either arm can be used to monitor onset of neuromuscular blockade in chronic renal failure patients with an arterio-venous shunt in the hand for haemodialysis.

Adult↗
PubMed1990

[Effect of cimetidine on neuromuscular blockade by succinylcholine and pancuronium].

The effect of cimetidine on neuromuscular blockade by succinylcholine and pancuronium was investigated in 54 adult patients scheduled for elective surgery. The neuromuscular blocking properties were estimated with single twitch height (T1) which was obtained by measuring the acceleration of adduction of the thumb in response to the ulnar nerve stimulation under N2O-fentanyl anesthesia. In cimetidine group, cimetidine 200 mg was administered orally on the night before surgery and 90 mins before anesthesia. Succinylcholine 1 mg.kg-1 (n = 14) or 1.5 mg.kg-1 (n = 20) was injected intravenously, and the onset time (from injection to 0% T1), the duration of maximal block (0% T1), and the recovery time from injection to 50% and 75% of control twitch height were evaluated. ED25 and ED50 of pancuronium were calculated from the dose response curve obtained by incremental administration of the drug (n = 20) whose total cumulative dose was 0.1 mg.kg-1. The recovery index of pancuronium was determined by measuring the 25%-75% recovery time. There was no significant difference between cimetidine pretreated patients and non-pretreated patients regarding these parameters of neuromuscular blockade with both succinylcholine and pancuronium. In conclusion, cimetidine has no influence on neuromuscular blockade of succinylcholine and pancuronium under N2O-fentanyl anesthesia.

Adolescent↗
PubMed1996

Assessment of sedation, analgesia, and neuromuscular blockade in the perioperative period.

Identification of adequate pain relief, sedation, and neuromuscular blockade in the perioperative period (be it for monitored anesthesia care, conscious sedation, ICU analgesia or sedation, or during intraoperative care) continues to be a challenge. Current subjective and objective techniques have been reviewed. The combination of clinical judgement, physiological response, and selected monitoring tools provide the current standard of care used to optimize patient care and comfort. Future directions in assessing pain control, adequacy of sedation, and degree of neuromuscular blockade include: (1) simplified scoring scales, (2) computerized analysis of the EEG, (3) computerized evoked potentials, (4) portable accelerography of electromyography for determination of neuromuscular blockade, and (5) closed loop system for delivery of analgesics, sedatives, and paralytics.

Analgesia↗
PubMedDate not supplied

Effect of neuromuscular blockade on energy expenditure in patients with severe head injury.

BACKGROUND: The purpose of this study was to determine the effect of neuromuscular blockade on energy expenditure in severely head-injured patients; to determine the effects of body temperature, nutrition support, and morphine use on metabolic rate; and to compare measured energy expenditure with values from predictive equations. METHODS: Energy expenditure was measured using indirect calorimetry in 2 groups of ventilated patients-18 with severe head injury during and after administration of pancuronium bromide and morphine, and second, 14 severely traumatized patients without severe head injury (trauma group) who received morphine without neuromuscular blockade. RESULTS: The mean energy expenditure of head-injured patients increased significantly once pancuronium was discontinued, ie, from 24.2 +/- 3.1 to 28.7 +/- 4.6 kcal/kg (p = .002). This effect was independent of other relevant variables such as morphine dose, body temperature, and nutrition support. When compared with the Harris-Benedict and World Health Organization predictive equations, neuromuscular blockade resulted in a stress factor of only 0.96 and 0.95, respectively, which increased to 1.19 and 1.18, respectively, once blockade was discontinued. Head-injured patients not on neuromuscular blockade had a significantly greater energy expenditure when compared with the trauma group (p = .02). CONCLUSIONS: Neuromuscular blockade in severely head-injured patients decreases energy expenditure to basal levels, independent of morphine use, body temperature, and feeding. Levels of hypermetabolism in both the head-injured and trauma groups were relatively low, at 19% and 5% above predicted values, respectively. This study provides useful information for the management of nutrition support in severely traumatized patients.

Adolescent↗
PubMedDate not supplied

Interaction of antibiotics on pipecuronium-induced neuromuscular blockade.

STUDY OBJECTIVE: To measure the interaction of two antibiotics (clindamycin and colistin) on neuromuscular blockade induced by pipecuronium bromide (a new long-acting, steroidal, nondepolarizing neuromuscular blocking drug). DESIGN: Prospective, randomized, placebo-controlled study. SETTING: Inpatient gynecologic and gastroenterologic service at a university medical center. PATIENTS: Three groups of 20 ASA physical status I and II patients with normal kidney and liver function, taking no medication, and undergoing elective surgery under general anesthesia. INTERVENTIONS: Anesthesia was induced with propofol and alfentanil intravenously (IV) and maintained with a propofol infusion and 60% nitrous oxide in oxygen. Pipecuronium bromide 50 micrograms/kg was administered after reaching a stable baseline of single-twitch response. At 25% recovery of pipecuronium-induced neuromuscular blockade, patients received one of two antibiotics, clindamycin 300 mg or colistin 1 million IU, or a placebo. MEASUREMENTS AND MAIN RESULTS: The recovery index (RI, defined as time from 25% to 75% recovery of neuromuscular blockade) was measured using the single-twitch response of the adductor pollicis muscle with supramaximal stimulation of the ulnar nerve at the wrist. RI after administration of an antibiotic (given at 25% recovery) was measured and compared with RI of the control group using Student's unpaired t-test. Statistical analyses of the results showed a significant prolongation of the recovery time (from 25% to 75% recovery) of 40 minutes for colistin. CONCLUSIONS: When this type of antibiotic is used during anesthesia with pipercuronium as a muscle relaxant, one must be aware of a significant prolongation of an already long-acting neuromuscular blockade and (although not observed in this study) possible problems in antagonism.

Adolescent↗
PubMed1979

Plasma concentrations of pancuronium and neuromuscular blockade after injection into the isolated arm, bolus injection, and continuous infusion.

To establish whether the plasma concentration of pancuronium reflects magnitude of neuromuscular blockade, the authors determined times of recovery from neuromuscular blockade and associated plasma concentrations following equipotent doses of pancuronium using three methods of pancuronium administration: the isolated-arm technique in conscious volunteers (n = 4), and the bolus intravenous injection (n = 7) and continuous-infusion methods (n = 3) in anesthetized patients. Although maximum depressions of twitch tension were similar (85 +/- 11,91 +/- 6, and 92 +/- 4 per cent, respectively) with the three techniques, times to recovery from neuromuscular blockade differed significantly, being 10 +/- 2 min with the isolated-arm technique, 23 +/- 7 min with the bolus-injection technique, and 46 +/- 5 min with the continuous-infusion method. The plasma concentration of pancuronium necessary for neuromuscular blockade was least with the isolated-arm technique and greatest with continuous infusion. At 25 and 75 per cent recovery, mean plasma concentrations were 0.07 +/- 0.01 and 0.04 +/- 0.01 microgram/ml in the isolated arm; 0.13 +/- 0.04 and 0.09 +/- 0.02 microgram/ml after bolus injection, and 0.20 +/- 0.04 and 0.11 microgram/ml during continuous infusion, respectively. It is concluded that the relationship between plasma concentration of pancuronium and magnitude of neuromuscular blockade depends on the method of pancuronium administration.

Humans↗
PubMedDate not supplied

Response to pancuronium after loss of atracurium-induced neuromuscular blockade.

OBJECTIVE: To describe a previously unreported event in which a patient became refractory to atracurium-induced neuromuscular blockade, but subsequently was adequately paralyzed with a standard dosage of pancuronium. CASE SUMMARY: A previously healthy 17-year-old woman who sustained multiple trauma developed tolerance to an atracurium infusion she was receiving while undergoing mechanical ventilation. On day 3 of neuromuscular blockade, she became unresponsive to atracurium as evidenced by excessive physical movement, increased peak airway pressures, and overbreathing assist control ventilation. Repeat boluses and increases in the atracurium infusion rate to a maximum of 1.27 mg/kg/h failed to provide a desired clinical response. A bolus dose of pancuronium 0.15 mg/kg was administered and the constant infusion was then changed to pancuronium 0.078 mg/kg/h. Within minutes, decreased respirations, peak airway pressures, and agitation were noted. The pancuronium infusion rate was then tapered to 0.045 mg/kg/h over 72 hours and continued to maintain adequate neuromuscular blockade. DISCUSSION: Potential pharmacokinetic and pharmacodynamic causes of loss of neuromuscular blockade in this patient are postulated. Possible explanations for loss of neuromuscular blockade include increased degradation of atracurium and/or a change in acetylcholine receptor physiology. CONCLUSIONS: The development of resistance to a specific neuromuscular blocking agent in the intensive care setting does not necessarily imply cross-tolerance or resistance to alternative agents. Also, loss of respiratory control by one neuromuscular blocking agent may be overcome by changing agents.

Adolescent↗
PubMed1990

Effect of epidurally administered bupivacaine on atracurium-induced neuromuscular blockade.

The effect of epidurally administered bupivacaine on duration, intensity and reversal characteristics of atracurium-induced neuromuscular blockade was studied in 30 healthy patients anaesthetized with thiopentone, fentanyl, midazolam and nitrous oxide. Fifteen patients received, in addition, epidural anaesthesia with bupivacaine. The remaining patients served as controls. The ulnar nerve was stimulated at the wrist and the evoked twitch response from the adductor pollicis was measured with a force displacement transducer. Neuromuscular blockade was induced with atracurium 0.5 mg i.v. and maintained with repeated doses of atracurium 0.15 mg/kg whenever the twitch height had recovered to 15% of the initial twitch height. After operation, the neuromuscular blockade was reversed with neostigmine when the twitch height had recovered to 15%. In the epidural group the clinical duration of neuromuscular blockade, time until first response to train-of-four (TOF) and reversal time were all significantly prolonged (P less than 0.05). Post-tetanic count (PTC) after 20 min was also significantly lower in the epidural group (P less than 0.05). It is therefore concluded that epidurally administered bupivacaine prolongs atracurium-induced neuromuscular blockade. The clinical implication of the modest prolongation is, however, limited.

Adult↗
PubMed1986

Frequency-dependence of neuromuscular blockade in the presence of d-tubocurarine.

The frequency-dependence of neuromuscular blockade in the presence of d-tubocurarine (dTC) was studied in the vascular perfused rat phrenic nerve-hemidiaphragm preparation by intracellular recording. Endplate potential (EPP) amplitude decreased as the frequency of stimulation increased (2.5-40 Hz). Additionally, the slopes of the regression lines of EPP amplitude versus the log of stimulation frequency decreased when the dTC concentration was increased. Since the dependence of neuromuscular blockade on frequency was not enhanced by higher concentrations of dTC, the postjunctional channel-blocking hypothesis does not sufficiently explain frequency-dependent neuromuscular blockade in the presence of dTC. However, the present results are compatible with the hypothesis that dTC influences neuromuscular blockade via a prejunctional action, affecting acetylcholine release.

Animals↗
PubMed2002

A comparison between anterior and posterior monitoring of neuromuscular blockade at the diaphragm: both sites can be used interchangeably.

UNLABELLED: We present a novel site of monitoring neuromuscular blockade of the diaphragm at the patient's back. After the induction of anesthesia, 12 patients were orotracheally intubated. Two Ag/AgCl-electrodes were attached at the right seventh or eighth intercostal space between the midclavicular and anterior axillary line; two Ag/AgCl-electrodes were paravertebrally attached on the right side lateral to vertebrae T12-L1 or L1-2. Two Ag/AgCl-skin-electrodes were placed over the right thenar area for an electromyography recording of the adductor pollicis (AP) muscle, and two Ag/AgCl-skin-electrodes were used to stimulate the ulnar nerve. Onset and offset of neuromuscular blockade after rocuronium 0.6 mg/kg were determined, and significant differences between diaphragm and AP muscle and agreement between the two methods were determined. Mean maximum block was more than 96% at all sites. Lag time, onset 50, and onset time were not significantly different between the diaphragm and the AP. However, time to reach 25% of control twitch was significantly longer at the AP muscle than at the diaphragm (P < 0.001). The difference of the means and limits of agreement between the anterior and the posterior site of diaphragmatic monitoring were 0 +/- 11 s, 3 +/- 9 s, 0 +/- 19 s, and -2% +/- 5% for lag, onset 50, onset time, and peak effect, respectively, and -2 +/- 2 min for the time to reach 25% of control twitch of neuromuscular blockade. We conclude that anterior and posterior diaphragmatic monitoring can be used interchangeably to determine neuromuscular blockade after rocuronium. IMPLICATIONS: We present a novel site of monitoring neuromuscular blockade of the diaphragm at the patient's back, which shows good agreement with the conventional anterior site at the seventh or eighth intercostal space.

Adult↗
PubMed1981

Pharmacokinetics of edrophonium and neostigmine when antagonizing d-tubocurarine neuromuscular blockade in man.

The pharmacokinetics and effectiveness of edrophonium antagonism of d-tubocurarine neuromuscular blockade were compared with that of neostigmine in surgical patients anesthetized with halothane and nitrous oxide. After an intravenous (iv) injection of d-tubocurarine (0.3 mg/kg), the single twitch tension was allowed to return to five per cent of the control level. Edrophonium, 0.5 or 1.0 mg/kg (n = 12), or neostigmine, 0.07 mg/kg (n = 6), was then given iv in combination with atropine, 1.0 mg, as a 2-min controlled infusion. Train-of-four and single twitch tension were followed for 60 min in all patients. Twelve patients were monitored for 90 min, six patients for 120 min, four patients for 150 min, and two patients for 240 min. Blood was sampled intermittently for four hours and assayed for edrophonium or neostigmine using high-pressure liquid chromatography. Edrophonium was found to promptly antagonize the d-tubocurarine blockade. Twitch tension rapidly increased to a plateau (a rate of increase in twitch tension of less than 2 per cent of control per min) which was sustained in all cases. The mean time to plateau for edrophonium was 2.9 +/- 0.21 (+/-SE) min as compared to 6.1 +/- 0.75 min for neostigmine. Neuromuscular blockade did not reappear in any patient. The degree of antagonism of the neuromuscular blockade by neostigmine and edrophonium was not significantly different. Except for a longer distribution half-life, the pharmacokinetic variables for edrophonium did not differ significantly from those for neostigmine. The elimination half-lives of edrophonium and neostigmine were 110 +/- 34 min (mean +/- SD) and 77 +/- 47 min, respectively. The authors therefore conclude that edrophonium, 0.5-1.0 mg/kg, has pharmacokinetic variables comparable to neostigmine and produces prompt, sustained, and effective antagonism of d-tubocurarine neuromuscular blockade.

Adult↗
PubMed1976

Mechaism of neuromuscular blockade with some antiepileptic drugs.

Effects of four antiepileptic drugs, viz., diphenylhydantoin, trimethadione, phenobarbitone and ethosuximide, were studied on different in vitro and in vivo skeletal muscle preparations which consisted of frog rectus, rat phrenic nerve diaphragm and cat gastrocnemius sciatic nerve preparations. A dose related blockade of neuromuscular transmission was seen with all the compounds tested. The blockade was mainly confined to the neuromuscular junction, although direct stimulation of muscle was slightly affected. The blockade was partially antagonized by physostigmine, adrenaline, succinylcholine, choline, tetraethylammonium and KCl and was additive to that due to tubocurarine. Moreover, the drugs were found to possess moderate local anaesthetic activity. The blockade was therefore considered to be partly due to curariform activity and partly due to their local anaesthetic activity.

Abdominal Muscles↗
PubMed2003

The effect of neuromuscular blockade on the efficiency of mask ventilation of the lungs.

We conducted a two-part study to assess the practice of withholding neuromuscular blockade until the ability to ventilate the lungs using a bag and face mask (mask ventilation) has been established following induction of anaesthesia. The first part of the study consisted of a postal survey (71% response rate) of 188 anaesthetists in the Oxford region to assess their current practice. Thirty per cent of respondents always checked mask ventilation before administering a neuromuscular blocking drug, whereas 39% of respondents (all them consultants) never did this. A further 31% only did so in the case of known or anticipated difficulty with the airway. In the second part of the study, we measured inspired (V(TI)) and expired (V(TE)) tidal volumes before and after neuromuscular blockade in 30 patients undergoing general anaesthesia. The ratio V(TE)/V(TI) was used as a measure of the efficiency of ventilation. There was no difference in V(TE)/V(TI) before [mean (SD) 0.47 (0.13)] and after [0.45 (0.13)] neuromuscular blockade. We conclude that neuromuscular blockade does not affect the efficiency of mask ventilation in patients with normal airways.

Adolescent↗
PubMedDate not supplied

Drug-induced neuromuscular blockade and myasthenia gravis.

Myasthenia gravis is an uncommon disorder of the neuromuscular junction resulting in weakness of all striated voluntary muscles. Therapeutic advances have increased patients' age and survival. Older patients with myasthenia gravis may have additional medication needs. Numerous drugs have experimental and clinical evidence of neuromuscular blockade. A MEDLINE search of the English literature from 1966 to the present pertinent to drug-induced myasthenia gravis was performed. Additional literature was obtained from reference citations of relevant articles. Drugs with several reports of neuromuscular blockade were assessed for causality by a recognized probability scale. Prednisone was most commonly implicated as aggravating myasthenia gravis, and D-penicillamine was most commonly associated with myasthenic syndrome. The greatest frequency of drug-induced neuromuscular blockade was seen with aminoglycoside-induced postoperative respiratory depression. However, drugs most likely to impact myasthenic patients negatively are those used in the treatment of the disease. These include overuse of anticholinesterase drugs, high-dose prednisone, and anesthesia and neuromuscular blockers for thymectomy.

Drug-Related Side Effects and Adverse Reactions↗
PubMed1996

Response to double-burst appears before response to train-of-four stimulation during recovery from non-depolarizing neuromuscular blockade.

BACKGROUND: Double-burst stimulation (DBS) it a relatively new nerve stimulation mode introduced for improved manual detection of residual neuromuscular blockade. Previous studies have shown that DBS3,3 50/50 (3 stimuli at 50 Hz followed 0.75 seconds later by 3 stimuli at 50 Hz) can detect deeper degrees of neuromuscular blockade than train-of-four (TOF) stimulation. AIM: The aim of the present study was to examine if DBS3,3 80/40 (3 stimuli at 80 Hz followed 0.750 s later by 3 stimuli at 40 Hz) can detect even deeper degrees of neuromuscular blockade than DBS3,3 50/50 and to determine the time lapse from reappearance of response to each of the two DBS modes until reappearance of response to the TOF mode of nerve stimulation. METHODS: The study comprised 20 women undergoing gynaecological surgery and anaesthetised with fentanyl, thiopentone, halothane, and nitrous oxide. Neuromuscular transmission was monitored by using mechanomyography and stimulation of the ulnar nerve. Atracurium was used for neuromuscular blockade. RESULTS: Elapsed time from reappearance of response to DBS3,3 80/40 and DBS3,3 50/50 to reappearance of response to TOF stimulation was 459 +/- 196 (mean +/- SD) and 360 +/- 150 seconds, respectively, (P < 0.05). CONCLUSIONS: DBS3,3 80/40 is capable of detecting deeper degrees of blockade than DBS3,3 50/50, which again is capable of detecting deeper degrees of blockade than TOF.

Adolescent↗