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Results for “Neuromuscular Blockade”

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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↗

PubMed2005

Tetanic stimulation of the peripheral nerve before transcranial electrical stimulation can enlarge amplitudes of myogenic motor evoked potentials during general anesthesia with neuromuscular blockade.

BACKGROUND: Neuromuscular blockade can suppress myogenic motor evoked potentials (MEPs). The authors hypothesized that tetanic stimulation (TS) of the peripheral nerve before transcranial stimulation may enhance myogenic MEPs during neuromuscular blockade. In the current study, the authors evaluated MEP augmentations by TS at different levels of duration, posttetanic interval, neuromuscular blockade, and stimulus intensity. METHODS: Thirty-two patients undergoing propofol-fentanyl-nitrous oxide anesthesia were examined. Train-of-five stimulation was delivered to C3-C4, and MEPs were recorded from the abductor hallucis muscle. In study 1, TS with a duration of 1, 3, or 5 s was delivered at 50 Hz to the tibial nerve 1, 3, or 5 s (interval) before transcranial stimulation, and the effects of TS on MEP amplitude were evaluated. In study 2, TS-induced MEP augmentations were evaluated at the neuromuscular blockade level (%T1) of 50% or 5%. In study 3, MEP augmentations by TS at stimulus intensities of 0, 5, 25, and 50 mA were evaluated. RESULTS: The application of TS significantly enlarged the amplitudes of MEPs at the combinations of duration (3, 5 s) and interval (1, 3, 5 s) compared with those without TS. TS-induced MEP augmentations were similarly observed at %T1 of both 50% and 5%. TS-induced MEP augmentations were observed at stimulus intensities of 25 and 50 mA. CONCLUSIONS: The results indicate that TS of the peripheral nerve before transcranial stimulation can enlarge the amplitude of MEPs during general anesthesia with neuromuscular blockade. TS of the peripheral nerve can be intraoperatively applied as a method to augment myogenic MEP responses.

Aged↗

PubMed2006

Analgesia, sedation and neuromuscular blockade in mechanically ventilated cardiac intensive care unit patients. Part III--Neuromuscular blockade.

This article reviews relevant clinical issues regarding sedation, analgesia and neuromuscular blockade in the cardiac intensive care unit, including monitoring tools and available therapeutic options. The pathophysiologic implications of pain, agitation, anxiety and delirium in the ventilated patient are also discussed. Although guidelines for sedation, analgesia and neuromuscular blocking drugs in critical care have recently been published, there is great variability in clinical practice. The complexity of the environment and associated pathologies makes it difficult to implement universally applicable therapeutic regimens. Knowledge of pharmacologic mechanisms is an important tool in the development of dynamic protocols adapted to each unit. Strategies that include monitoring resources are essential for the optimization of sedation, analgesia and neuromuscular blockade.

Analgesia↗

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↗

PubMed2006

The predisposition to inspiratory upper airway collapse during partial neuromuscular blockade.

RATIONALE: Partial neuromuscular transmission failure by acetylcholine receptor blockade (neuromuscular blockade) or antibody-mediated functional loss (myasthenia gravis), even with a magnitude of muscle weakness that does not evoke respiratory symptoms, can evoke dysphagia and decreased inspiratory airflow, and increases the risk of susceptible patients to develop severe pulmonary complications. OBJECTIVES: To assess whether impaired neuromuscular transmission predisposes individuals to inspiratory upper airway collapse, we assessed supraglottic airway diameter and volume by respiratory-gated magnetic resonance imaging, upper airway dilator muscle function (genioglossus force and EMG), and changes in lung volume, respiratory timing, and peripheral muscle function before, during, and after partial neuromuscular blockade in healthy, awake volunteers. MEASUREMENTS AND MAIN RESULTS: Partial neuromuscular blockade (train-of-four [TOF] ratio: 0.5 and 0.8) was associated with the following: (1) a decrease of inspiratory retropalatal and retroglossal upper airway volume to 66 +/- 22 and 82 +/- 12% of baseline, which was significantly more intense in the retropalatal area; (2) an attenuation of the normal increase in anteroposterior upper airway diameter during forced inspiration to 74 +/- 18% of baseline; (3) a decrease in genioglossus activity during maximum voluntary tongue protrusion to 39 +/- 19% (TOF, 0.5) and 73 +/- 29% (TOF, 0.8) of baseline; and (4) no effects on upper airway size during expiration, lung volume, and respiratory timing. CONCLUSIONS: Thus, impaired neuromuscular transmission, even to a degree insufficient to evoke respiratory symptoms, markedly impairs upper airway dimensions and function. This may be explained by an impairment of the balance between upper airway dilating forces and negative intraluminal pressure generated during inspiration by respiratory "pump" muscles.

Adult↗

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↗

PubMed2002

[Plasma cholinesterase variations as a result of prolonged neuromuscular blockade. Review and problems encountered in two cases of prolonged neuromuscular blockade after muscle relaxation with succinylcholine as compared to mivacurium].

Succinylcholine and mivacurium are degraded more slowly in patients with a qualitatively or quantitatively reduced plasma cholinesterase and are therefore known for inducing a prolonged postoperative apnea. Perioperative laboratory screening even including plasma cholinesterase activity testing will not prevent this due to a possible aberration only in the qualitative cholinesterase activity. This is illustrated by introducing two cases reports of prolonged apnea after administration of mivacurium or succinylcholine. The pathophysiology of plasma cholinesterase is reviewed including genetically determined variants and the degradation pathways of mivacurium and succinylcholine. Only extensive laboratory chemical tests are sufficient to prevent this possible complication. Due to the rare incidence there is no evidence for recommending these laboratory investigations in all patients. Once prolonged apnea occurs following the administration of mivacurium or succinylcholine the best choice is ongoing ventilation combined with a sufficient sedation.

Apnea↗

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↗

PubMedDate not supplied

Neuromuscular blockade in children.

Neuromuscular blocking agents (NMBAs) have been widely used to control patients who need to be immobilized for some kind of medical intervention, such as an invasive procedure or synchronism with mechanical ventilation. The purpose of this monograph is to review the pharmacology of the NMBAs, to compare the main differences between the neuromuscular junction in neonates, infants, toddlers and adults, and moreover to discuss their indications in critically ill pediatric patients. Continuous improvement of knowledge about NMBAs pharmacology, adverse effects, and the many other remaining unanswered questions about neuromuscular junction and neuromuscular blockade in children is essential for the correct use of these drugs. Therefore, the indication of these agents in pediatrics is determined with extreme judiciousness. Computerized (Medline 1990-2000) and active search of articles were the mechanisms used in this review.

Adult↗

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↗

PubMed2005

Drugs to facilitate recovery of neuromuscular blockade and muscle strength.

Several drugs that quicken recovery from neuromuscular blockade caused by vecuronium in anesthetized patients are reviewed. Ulinastatin, a protease inhibitor, is thought to promote the release of acetylcholine at the neuromuscular junction and increases hepatic blood flow and urine volume. For this reason, ulinastatin quickens recovery from neuromuscular blockade in anesthetized patients receiving vecuronium. Additionally, pretreatment with ulinastatin avoids prolongation of vecuronium-induced neuromuscular blockade in patients with hepatic cirrhosis. Gabexate mesilate is also a protease inhibitor. During a continuous infusion of gabexate mesilate, recovery from neuromuscular blockade was quickened. Amino acid-enriched solution supplies energy to the skeletal muscles and causes an increase in muscle strength. An infusion of amino acid-enriched solution hastens recovery from neuromuscular blockade in anesthetized patients. When amino acids supply energy to the skeletal muscles, they simultaneously produce heat in the skeletal muscles. This thermal generation may be closely related to fast recovery from neuromuscular blockade. Amino acid-enriched solution makes recovery from neuromuscular blockade quick and avoids hypothermia during general anesthesia. Milrinone, a phosphodiesterase III inhibitor, is supposed to increase the release of acetylcholine at the neuromuscular junction and make the neuromuscular junction sensitive to acetylcholine. Therefore, recovery from neuromuscular blockade is hastened. Nicorandil enhances membrane K+ conductance in skeletal muscle and increases contraction of the skeletal muscle. Thus, nicorandil quickens recovery from neuromuscular blockade.

Amino Acids↗

PubMedDate not supplied

Mastering neuromuscular blockade.

Learn how neuromuscular blocking agents work and how to assess and manage a patient receiving these drugs.

Analgesics, Opioid↗

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↗

PubMed2001

Intramuscular versus surface electromyography of the diaphragm for determining neuromuscular blockade.

We determined the neuromuscular blockade of 0.2 mg. kg(-1) mivacurium at the diaphragm by using two new methods of electromyographic (EMG) monitoring and compared it with acceleromyography of the orbicularis oculi (OO) and the corrugator supercilii (CS) muscle. After the induction of anesthesia in 15 patients undergoing gynecologic laparoscopic surgery, evoked EMG responses at the diaphragm were obtained by using skin electrodes at the back of the patient, placed lateral to T12/L1 or L1/L2, and a laparoscopically applied wire electrode inserted into the dorsolateral portion of the diaphragm. Acceleromyography at the right OO and the left CS was performed. The facial and phrenic nerves were stimulated transcutaneously (onset: every 10 s, offset: every 15 s, single twitch stimulation). Lag and onset time, peak effect, and clinical duration (time to reach 75% of control value and time to reach 90% of control value) were measured and the results were compared by using analysis of variance; P < 0.05 showed significant difference. Pearson's correlation test and the Bland-Altman test were used to compare the two diaphragmatic monitoring methods. Mean peak effects of >98% were reached at all sites. Onset times at diaphragm (skin, IM) were significantly (P < 0.005) shorter than at the CS or OO (100 +/- 14 s and 98 +/- 16 s vs 147 +/- 39 s, 185 +/- 38 s) without being statistically different between OO and CS. There was a good correlation of lag, onset time, time to reach 75% of control value, and time to reach 90% of control value (r = 0.8, 0.9, 0.8, and 0.75; P < 0.01) between the two diaphragmatic methods. Mean difference and limits of agreements are -2 +/- 15 s, 1 +/- 21 s, -1 +/- 2.3 min, and -2 +/- 3.4 min. We showed a shorter onset and clinical duration at the diaphragm in comparison with CS and OO. Two methods of EMG of the diaphragm correlated well and showed good comparability. The novel method of surface diaphragmatic EMG at the patient's back may be useful during routine clinical anesthesia.

Adolescent↗