Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuromuscular Blockade”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1976

Clindamycin enhances a nondepolarizing neuromuscular blockade.

Neuromuscular blockades induced by clindamycin alone and with d-tubocurarine or pancuronium were examined in the in-vitro guinea pig lumbrical muscle-nerve preparation. Clindamycin, 80-240 mug/ml, initially increased twitch tension. With higher concentrations (180-240 mug/ml) twitch tension subsequently decreased. With 15 to 20 per cent depression of twitch tension by clindamycin, neostigmine (5-20 ng/ml) or calcium (81 mug/ml) slightly but not completely antagonized the blockade. Clindamycin, 40 mug/ml, a dose that did not depress twitch tension, potentiated d-tubocurarine- or pancuronium-induced neuromuscular bloackade. Plasma concentrations of clindamycin of 10-40 mug/ml were recommended for treating serious infections. The authors conclude that the administration of clindamycin may augment nondepolarizing blockade in man, and antagonism by neostigmine and calcium may be incomplete.

Adjuvants, Anesthesia↗
PubMed1995

Cardiopulmonary implications of neuromuscular blockade.

Neuromuscular blocking agents (NMBAs) are used to facilitate mechanical ventilation in critically ill patients. Individual NMBAs differ in their metabolism and elimination, side effects, and duration of action. These differences help designate which NMBA has the greatest efficacy, given different scenarios. A common theme with all NMBAs is their ability to ablate spontaneous breathing; hence, vigilant cardiopulmonary monitoring is warranted when NMBAs are used.

Critical Care↗
PubMed1998

Respiratory function in children during recovery from neuromuscular blockade.

Residual neuromuscular blockade is a major risk factor for respiratory insufficiency. We examined the relationship between neuromuscular and respiratory function in 18 ASA I or II children aged 2-4 years. Lung function was measured by pneumotachography and transpulmonary pressure, neuromuscular transmission by first twitch response ratio (T1:T1) and train-of-four ratio (TOFR), before and at specific points in recovery from vecuronium paralysis. The tidal volume was directly related to maximal inspiratory pressure at occlusion (PIOCC), P < 0.001, whereas the minute ventilation (VE) was related to the respiratory drive (P0.1), P < 0.001. The best predictors of minute ventilation were the P0.1 (r = 0.57), and the TOFR (r = 0.62). PIOCC and P0.1 correlated closely (r = 0.889, P = 0.002) but TOFR and T1:T1 did not correlate with either. Our results show that the occlusion pressure measurements, P0.1 and PIOCC, were good predictors of both VE.kg-1 and respiratory work.

Anesthesia Recovery Period↗
PubMed1995

AAEM case report #29: Prolonged paralysis after neuromuscular blockade.

Nondepolarizing neuromuscular blocking agents (NMBA) are being used with increasing frequency in critically ill patients. Recently, many centers have described patients with prolonged muscle weakness after long-term use of these agents, either alone or in combination with other agents or disorders. Brief weakness lasting several hours to several days is probably the result of prolonged neuromuscular blockade, while more prolonged weakness lasting several weeks to months is, in all likelihood, caused by a myopathy. Patients with this myopathic disorder have flaccid paralysis with intact cognition and sensation. Electrodiagnostic findings include decreased M-wave amplitudes, positive waves and fibrillations, and rapid recruitment of small amplitude short duration, polyphasic motor unit potentials. Muscle biopsy findings include atrophy of type I and type II fibers, myofiber necrosis, and selective loss of thick myofilaments. The myopathy is believed to be related to the prolonged use of NMBA either alone or in combination with other disorders or medications, particularly corticosteroids. The weakness experienced by these patients leads to additional respiratory compromise, difficulty weaning from the ventilator, and prolonged hospitalization.

Adrenal Cortex Hormones↗
PubMed1995

A bolus plus continuous infusion protocol for controlling neuromuscular blockade during anesthesia.

Neuromuscular blockade is controlled during anesthesia by administering either bolus doses or a continuous infusion of a blocking agent. To test whether a constant infusion technique requires less attention and provides better control we used a computer to simulate neuromuscular blockade. Using the model we maintained 95% blockade with mivacurium, atracurium, and vecuronium. It required 1.2 changes per hour to maintain the blockade by continuous infusion; an average of 4.5 bolus per hour were required to maintain blockade by the bolus technique. When the bolus and continuous infusion techniques were combined, only 0.16 changes per hour were required. Atracurium was then given to ten patients during anesthesia, following the bolus plus continuous infusion protocol. After a bolus was given to obtain 100% twitch depression, for tracheal intubation, neuromuscular function was assessed by train-of-four stimulation of the ulnar or facial nerves by observing the resultant muscle movement. When the first twitch of the train-of-four returned, relaxation was maintained by continuous infusion. A bolus was given and the drug infusion rate was changed whenever the level of relaxation changed from the desired one twitch of the train-of-four. The infusion rate was adjusted only 1.12 +/- 0.79 times per hour. The desired level of muscle relaxation was easily controlled using the bolus plus continuous infusion protocol. The infusion scheme might be implemented in future drug infusion pumps.

Adult↗
PubMed1994

Edrophonium for the antagonism of neuromuscular blockade in dogs.

Neuromuscular, electrocardiographic and autonomic nervous changes were studied when edrophonium and four combinations of edrophonium and atropine were used to antagonise vecuronium-induced neuromuscular blockade in 87 dogs anaesthetised with halothane. Edrophonium (500 micrograms/kg body-weight) was given alone, or with atropine (40 micrograms/kg) or one minute after a dose of 600 micrograms of atropine, and a lower dose of edrophonium (250 micrograms/kg) was used with high (40 micrograms/kg) and low (20 micrograms/kg) doses of atropine. The neuromuscular blockade was antagonised when some recovery was present. The reversal was rapid and complete in 75 cases, but the remaining 12 dogs which received the low dose of edrophonium required a second injection. Trials with the high dose of edrophonium alone were discontinued because cardiac arrest occurred in one dog and bronchosecretion with profuse salivation in another. The heart rate increased with the low dose of edrophonium and the high dose of atropine, and increased and then decreased when edrophonium was followed by 600 micrograms of atropine. The heart rate was stable when the high and low doses of atropine and edrophonium were matched. All the treatments caused atrioventricular blockade. Non-cardiac autonomic changes (salivation and bronchosecretion) occurred in only two of the 87 dogs.

Anesthesia, Intravenous↗
PubMed1996

Use of peripheral nerve stimulators to monitor patients with neuromuscular blockade in the ICU.

BACKGROUND: Neuromuscular blockade is a frequently used therapy in the ICU. However, recent reports of prolonged paralysis and general muscular weakness in patients treated with this procedure have raised concerns about its use in intensive care. OBJECTIVE: The purpose of this study was to assess current monitoring practices of nurses who care for patients treated with neuromuscular blockade. METHODS: In January 1995, questionnaires were mailed to a random national sample of 2000 critical care nurses. Of the 2000 questionnaires mailed, 744 were returned. RESULTS: The number of patients per month who were treated with neuromuscular blockade in ICU settings ranged from 0 to 75 (mean = 6.82, SD = 9.15). For each patient, the average number of days of blockade ranged from less than 1 to 63 (mean = 4.12, SD = 3.36). The most common indications for neuromuscular blockade were to assist in mechanical ventilation, reduce oxygen consumption, and treat agitation. Only 41% of respondents (n = 306) reported using train-of-four stimuli and a peripheral nerve stimulator to monitor patients. Depth of neuromuscular blockade was routinely monitored by using clinical assessment (31%), a peripheral nerve stimulator (16%), or both (52%). CONCLUSIONS: Among the respondents, variations existed in monitoring practices and in the use of peripheral nerve stimulators, including the frequency of monitoring and use of the baseline milliamperage. Appropriate monitoring and titration of neuromuscular blocking agents by ICU nurses may aid in preventing adverse effects, including the potential for prolonged neuromuscular blockade. The existing variations in practice may affect patients' outcomes.

Critical Care↗
PubMed1989

Intravenous ranitidine antagonizes intense atracurium-induced neuromuscular blockade in rats.

The neuromuscular action of ranitidine, an H2-receptor antagonist, was investigated by determining its effect on atracurium-induced neuromuscular blockade in urethane-anesthetized and mechanically ventilated male Sprague-Dawley rats. An intravenous bolus and an infusion of atracurium were administered to produce a stable 93 +/- 5% (n = 11) neuromuscular blockade as judged by tibialis anterior muscle twitch response. Ranitidine administered as a 1, 5, or 10 mg/kg normal body weight IV bolus during continuous atracurium infusion produced marked antagonism of neuromuscular paralysis. The percentage of antagonism (25 +/- 9%; n = 4; 53 +/- 19%, n = 4; and 79 +/- 9%, n = 3, respectively) was linearly related to the dose of ranitidine (r = 0.86, P less than 0.05). These results suggest that IV ranitidine has a significant anticholinesterase action against atracurium-induced neuromuscular blockade.

Animals↗
PubMed1995

Prolonged paralysis after neuromuscular blockade.

Non-depolarizing neuromuscular blocking agents have been used with increasing frequency in critically ill patients. Recently, numerous reports have described patients with prolonged muscle weakness after use of these agents for more than two days. Brief weakness lasting several hours to several days is likely the result of prolonged neuromuscular blockade, while more prolonged weakness lasting several weeks to months is likely caused by a myopathy. Specific features of this myopathic disorder are reviewed. Clinically, patients have flaccid paralysis with intact sensation and cognition. Electrodiagnostic findings include decreased M-wave amplitudes, mild positive waves and fibrillations and small, polyphasic motor unit potentials. Muscle biopsy findings include atrophy of type I and type II fibers, myofiber necrosis and selective loss of thick myofilaments. This myopathic disorder is felt to be related to the prolonged use of non-depolarizing neuromuscular blocking agents either alone or in combination with other medications or disorders. Many authors feel that the disorder is caused specifically by a combination of prolonged neuromuscular blockade and corticosteroids. Selective loss of thick myofilaments on muscle biopsy has been produced experimentally in rats by combing denervation with high doses of corticosteroids. As this disorder likely leads to additional respiratory compromise, difficulty weaning from the ventilator, and prolonged hospitalization, prevention is warranted. Methods of prevention include minimizing the dosage of non-depolarizing neuromuscular blocking agents and of other drugs with an effect on the neuromuscular junction, twitch monitoring with a peripheral nerve stimulator and allowing patients to come to an unparalyzed state for brief periods.

Adrenal Cortex Hormones↗
PubMed1987

Changes in the power spectrum of the evoked compound action potential of the adductor pollicis with the onset of neuromuscular blockade.

The effects of neuromuscular blockade by atracurium and vecuronium on the power spectrum of the evoked compound action potential (ECAP) of the adductor pollicis were investigated in 30 adult patients undergoing elective surgery. The changes in amplitude and mean power frequency (MPF) of the ECAP were measured. Ten patients received an ED95 (0.23 mg kg-1) of atracurium and 10 received an ED95 (0.055 mg kg-1) of vecuronium. The remaining 10 patients did not receive any neuromuscular blocking drug, and were monitored for 6 min to exclude any time-related changes in the ECAP. Neuromuscular blockade produced a decrease in total power and a shift towards lower frequencies. This was reflected in a decrease in the MPF in those patients receiving atracurium or vecuronium. There was no significant difference (P less than 0.05) between the atracurium and vecuronium groups in the magnitude of the change in MPF. These findings suggest that the previously reported increase in the duration of the negative deflection of the ECAP is predominantly the result of a change in its frequency components.

Action Potentials↗
PubMed1986

Verapamil intensifies neuromuscular blockade produced by gallamine and pancuronium at the chick neuromuscular junction.

Experiments were performed to study the effect of verapamil on neuromuscular transmission and muscle contraction at a chick skeletal muscle-nerve preparation. In addition, the effects and interactions of verapamil with some muscle relaxants were studied in the same preparation. These effects were explored by studying the effects of verapamil on: directly-and indirectly-elicited twitch contractions, and neuromuscular blockade produced by gallamine and pancuronium. The results showed that verapamil (2-200 microM) had a differential effect on the twitch responses; more reductions occurred in the indirectly-elicited twitch tension, whereas the directly-elicited twitch response was reduced only by 20-30% of maximum indirectly-elicited twitch tension. Furthermore, in low concentrations (1-20 microM), verapamil significantly increased the neuromuscular blockade produced by gallamine (28-1280 nM) and pancuronium (18-573 nM). In high concentrations (greater than 200 microM), verapamil completely blocked the indirectly-elicited twitch response and produced a marked contracture in the chick skeletal muscle (1.0 +/- 0.1 g, n = 6). It was concluded that by reducing twitch tension and inhibiting neuromuscular transmission, verapamil increases (intensifies) neuromuscular blockade produced by muscle relaxants, e.g. gallamine and pancuronium.

Animals↗
PubMed1997

[Effects of halothane and sevoflurane on reversal of neuromuscular blockade induced by vecuronium in man].

To evaluate residual effects of inhalational anesthetics after reversal of neuromuscular blocking agent, neuromuscular function was monitored after halothane or sevoflurane anesthesia in thirty-seven patients (ASA physical status I or II) for elective surgery after obtaining informed consent. Electromyograph of the adductor pollicis muscle in response to train of four (TOF) stimulation was monitored throughout the study. The first twitch of TOF (T1; % of its control) and the ratio of the fourth twitch to the first twitch of TOF (T4/T1; TR) were recorded at 0, 2, 5, 10, and 15 min after reversal. The patients were divided into five groups; 1) the fentanyl group (n = 7) received fentanyl/N2O; 2) in the halothane stop group (n = 6), halothane was discontinued at least fifteen minutes before neostigmine administration; 3) in the halothane stable group (n = 7), 0.7% halothane was maintained until fifteen minutes after neostigmine; 4) in the sevoflurane stop group (n = 12), sevoflurane was discontinued fifteen minutes before the reversal; 5) in the sevoflurane stable group (n = 5), 3% sevoflurane was maintained until fifteen minutes after the reversal. Anesthesia was induced by thiopental 4 mg.kg-1 and suxamethonium 1 mg.kg-1 and the patients were intubated. After initial dose of vecuronium 0.1 mg.kg-1, the additional dose of 0.02 mg.kg-1 was administered to maintain T1 under 10% of the control value. At the end of the surgery atropine 0.015 mg.kg-1 and neostigmine 0.04 mg.kg-1 were administered to reverse vecuronium when T1 had recovered to 25% of its control. Halothane groups did not differ from fentanyl group. Recovery of T1 at 15 min was suppressed after discontinuation of sevoflurane (86.0 +/- 8.2%) in comparison with fentanyl (97.0 +/- 8.3%). Both T1 (75.4 +/- 12.2%) and TR (68.0 +/- 12.6%) at 15 min after the reversal during 3% sevoflurane inhalation were below those of the stable group. We conclude that the residual sevofulrane after discontinuation of inhalation may impair the neuromuscular transmission after the reversal of neuromuscular blockade. Neuromuscular function should be monitored after the end of anesthesia even though the patient is fully awake.

Adult↗
PubMed1993

Effect of vecuronium-induced neuromuscular blockade on cortical motor evoked potentials.

BACKGROUND: Neuromuscular blockade (NMB) is a frequent component of anesthetic techniques used during surgery in which monitoring of the nervous system is desirable. Because NMB should affect the evoked muscle response to transcranial magnetic stimulation (tcMMEP), their relationship in a primate model was characterized. METHODS: Transcranial magnetic stimulation was characterized during NMB using an infusion of vecuronium in ten adult cynomologous monkeys during anesthesia with a continuous ketamine infusion. Neuromuscular blockade was measured by peak-to-peak amplitude of the evoked muscular activity (compound muscle action potential [m-response]) of the thenar muscles and mechanical muscle action (ratio of the fourth to first peak in the train of four [TOF]) after direct stimulation of the median nerve. Neuromuscular blockade was increased incrementally to complete block and then allowed to decrease until complete resolution of measurable block. Transcranial magnetic stimulation was assessed by measuring the onset latency (time from stimulation to beginning response) and amplitude of the thenar EMG response. Cortical stimulation was accomplished using a Cadwell MES-10 magnetic stimulator at 80% of full output (1.6 Tesla). RESULTS: The tcMMEP, m-response amplitude, and mechanical muscle action, unblocked, were reduced with increasing NMB. Transcranial magnetic stimulation amplitude was more variable than was onset latency. Transcranial magnetic stimulation amplitude reduction from the baseline value did not achieve statistical significance until the m-response amplitude was reduced to 0.2 of baseline or until the TOF ratio was reduced to 0.1. Transcranial magnetic stimulation onset latency prolongation from baseline was not significantly affected by declining TOF ratios, but was prolonged when the m-response declined to 0.1 of baseline. CONCLUSIONS: This study indicates that tcMMEP onset latency is not significantly affected by NMB if the degree of blockade in the muscles used for tcMMEP monitoring is not extreme (greater than 0.2 of baseline by m-response amplitude or a TOF ratio of 0.1 or greater). If monitoring of tcMMEP amplitude is desired, partial neuromuscular blockade may be acceptable. However, amplitude reduction may occur during partial NMB. Maintenance of a constant degree of NMB is suggested to minimize amplitude fluctuations.

Anesthesia, Inhalation↗
PubMed1991

Interactions of adenosine and vecuronium in neuromuscular blockade in cats.

The effect of adenosine on the neuromuscular blockade induced by vecuronium and the capacity of neostigmine to reverse this combined blockade were studied in 30 cats on a standard sciatic nerve--tibialis anterior muscle preparation. Adenosine infused to 6 cats at a constant rate (3.9 +/- 1.1 mg/kg/min) to produce a stable 50% reduction of the mean arterial pressure did not affect neuromuscular transmission. At the same 50% reduction of the mean arterial pressure by adenosine or sodium nitroprusside infusion in another 15 cats, adenosine (n = 9) significantly potentiated vecuronium-induced neuromuscular blockade, but sodium nitroprusside (n = 6) did not. Neostigmine antagonized the neuromuscular blockade of similar degrees produced either by the combination of adenosine with vecuronium in the above 9 cats or by vecuronium alone in the remaining 9 cats. There was no significant difference in the doses of neostigmine given. Because no potentiation was found at the same level of hypotension induced by sodium nitroprusside, the potentiation effect of adenosine on neuromuscular blockade is not likely to be due to the hypotensive effect of adenosine, but may be due to impairment, by adenosine, of acetylcholine release from motor nerve endings. We conclude that adenosine potentiates neuromuscular blockade by vecuronium and that neostigmine can be expected to reverse this combined blockade.

Adenosine↗
PubMed1999

Marked prolongation of the succinylcholine effect two hours after neostigmine reversal of neuromuscular blockade in a patient with chronic renal insufficiency.

Prolonged neuromuscular blockade from succinylcholine after neostigmine administration has been reported in patients with frank renal failure. We present a case of prolonged neuromuscular blockade from succinylcholine administration, given 2 hours after neostigmine reversal of neuromuscular blockade in a patient with chronic renal insufficiency. This case shows that patients with chronic renal insufficiency, like patients with renal failure, are at risk for prolonged succinylcholine blockade if they have recently received anticholinesterase reversal of neuromuscular blockade. Administration of succinylcholine for facilitation of urgent endotracheal intubation may be required soon after reversal of nondepolarizing muscle relaxants, particularly in patients who return to the operating room for emergency care.

Aged↗
PubMed1987

Monitoring neuromuscular blockade with calf stimulators.

The efficacy of monitoring neuromuscular blockade during surgery based on visual assessment of the response to calf stimulation was determined in twenty-five patients. The calf stimulator was adjusted before the administration of any muscle relaxant to produce a brisk ankle jerk. Following an initial bolus dose of atracurium (0.5 mg/kg), further incremental doses (0.2 mg/kg) were administered when the response to calf stimulation was small and obvious. The resultant neuromuscular blockade was judged to be adequate throughout the surgical procedures, with an average of five incremental doses of atracurium being administered. In the presence of neuromuscular blockade the response to calf muscle stimulation was often greater than that produced by supramaximal stimulation of the ulnar nerve with a peripheral nerve stimulator. The response to calf muscle stimulation often persisted after that resulting from ulnar nerve stimulation was abolished. The technique has only limited accuracy in assessing neuromuscular blockade. However, it may be useful in helping to avoid the wide fluctuations in blockade which are prone to occur with the intermediate duration competitive neuromuscular blocking agents.

Adult↗
PubMed1991

Effects of residual concentrations of isoflurane on the reversal of vecuronium-induced neuromuscular blockade.

Thirty-six anesthetized patients (ASA physical status 1 or 2) undergoing elective surgery were monitored (isometric adductor pollicis mechanical activity) to detect the effects of discontinuing isoflurane anesthesia upon the reversal of vecuronium-induced neuromuscular blockade. Neuromuscular blockade was produced by vecuronium 100 micrograms/kg and additional doses of 20 micrograms/kg until completion of surgery. The patients were randomly divided into three groups: in the control group (n = 12), only fentanyl/N2O was given; in the "isostable" group (n = 12), isoflurane at an end-tidal concentration of 1.25% was maintained throughout anesthesia; in the "isostop" group (n = 12), isoflurane 1.25% was discontinued before neostigmine administration. In all groups, paralysis was antagonized with 15 micrograms/kg intravenous (iv) atropine and 40 micrograms/kg iv neostigmine when the twitch height (0.1 Hz) had regained 25% of its control value. The measured parameters were twitch height, train-of-four, and 50--100-Hz tetanic fade. No significant differences were found among the three groups with respect to the final twitch heights and tetanic fades at 50 Hz. In the isostable group, final mean train-of-four was significantly less (75%) than in the other patients (88%) (P less than 0.01). Mean tetanic fade at 100 Hz was significantly less in the isostable group (31%) than in the isostop group (57%) (P less than 0.01) and control group (84%) (P less than 0.01). We conclude that discontinuing isoflurane anesthesia for 15 min improves the reversal of a vecuronium paralysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Edrophonium antagonizes combined lidocaine-pancuronium and verapamil-pancuronium neuromuscular blockade in cats.

The effects of lidocaine or verapamil on pancuronium neuromuscular blockade and the ability of anticholinesterase agents to antagonize these combined blockades were studied in 14 cats using a standard peroneal nerve-anterior tibialis muscle preparation. Pancuronium was infused at a constant rate to produce a stable 50% depression of single twitch tension. In nine cats, intravenous lidocaine boluses followed by a constant infusion produced serum lidocaine levels of 5.09 +/- 1.9 micrograms/ml (mean +/- SD) and resulted in an additional 20.0 +/- 5.5% depression of twitch tension. In the other five cats, intravenous injection of 0.15 mg/kg of verapamil produced an additional 12.8 +/- 8.0% twitch depression of pancuronium-induced neuromuscular blockade. For individual animals, edrophonium antagonism of the combined lidocaine-pancuronium-induced neuromuscular blockade or combined verapamil-pancuronium-induced neuromuscular blockade was not significantly different from antagonism of an equivalent twitch depression produced by pancuronium alone. It is concluded that lidocaine and verapamil augment neuromuscular blockade caused by pancuronium and that anticholinesterase antagonism of this augmented blockade can be expected to occur in a normal fashion.

Animals↗