Neuromuscular Blockade
Neuromuscular Blocking Agents
gamma-Cyclodextrins
Vecuronium Bromide
Pancuronium
Neuromuscular Nondepolarizing Agents
Androstanols
Neostigmine
Edrophonium
Atracurium
Tubocurarine
Succinylcholine
Ulnar Nerve
Decamethonium Compounds
Pipecuronium
Anesthesia Recovery Period
Nitrous Oxide
Delayed Emergence from Anesthesia
Neuromuscular Depolarizing Agents
Curare
Paralysis
Anesthesia, Inhalation
Anesthesia
Myography
Anesthesia, General
Enflurane
Laryngeal Muscles
Monitoring, Intraoperative
Isoquinolines
Nervous System Physiological Processes
Sesquiterpenes, Eudesmane
Cholinesterase Inhibitors
Diaphragm
Phrenic Nerve
Pyridostigmine Bromide
Preanesthetic Medication
Intubation, Intratracheal
Neuromuscular Monitoring
Halothane
Fentanyl
Muscle Contraction
Dose-Response Relationship, Drug
Gallamine Triethiodide
Facial Nerve
Anesthesia, Intravenous
Alkalosis, Respiratory
Electromyography
Isoflurane
Thiopental
Nerve Block
Conscious Sedation
Bungarotoxins
Monitoring, Physiologic
Respiration, Artificial
Propofol
Laryngeal Masks
Synaptic Transmission
Drug Interactions
Cats
Hypnotics and Sedatives
Anesthetics, Intravenous
Oximetry
Hypothermia, Induced
Lidocaine
Intensive Care
Anesthetics, Inhalation
Respiration
Respiratory Mechanics
Receptors, Cholinergic
Infusions, Intravenous
Hemodynamics
Are changes in the evoked electromyogram during anaesthesia without neuromuscular blocking agents caused by failure of supramaximal nerve stimulation? (1/235)
The evoked electromyogram often decreases during anaesthesia in the absence of neuromuscular block. We have measured the electromyogram of the first dorsal interosseous muscle evoked by train-of-four stimulation of the ulnar nerve in 63 patients undergoing anaesthesia for minor surgery. We used Medicotest P-00-S electrodes, a Datex Relaxograph and a current sink in the stimulating leads in parallel with the current path through the patient. The current sink was used to shunt some of the maximum available output current from the Relaxograph while maintaining the supramaximal stimulus current passing through the patient. After 30 min of anaesthesia, when the muscle response to train-of-four was stable, the ulnar nerve stimulus current was increased by reducing the proportion shunted through the current sink. The electromyographic response did not change during the study in 13 patients. In the remaining 50 patients, the response decreased to 78.4% (SD 27.1%, range 7.5-95.0%) of baseline values over the first 20 min of anaesthesia. In 22 of these patients, the electromyographic response increased from 71.4 (SD 22.6)% to 92.3 (9.5)% of baseline responses when the stimulus current was increased by 12.3 (2.4) mA, while in the remaining 28 patients the response decreased to 83.7 (10.6)% and did not increase with increasing stimulus current. These results suggest that loss of supramaximal stimulation is partly responsible for the observed changes in the evoked electromyogram during anaesthesia. (+info)Antagonism of vecuronium-induced neuromuscular block in patients pretreated with magnesium sulphate: dose-effect relationship of neostigmine. (2/235)
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. (+info)SI neuron response variability is stimulus tuned and NMDA receptor dependent. (3/235)
Skin brushing stimuli were used to evoke spike discharge activity in single skin mechanoreceptive afferents (sMRAs) and anterior parietal cortical (SI) neurons of anesthetized monkeys (Macaca fascicularis). In the initial experiments 10-50 presentations of each of 8 different stimulus velocities were delivered to the linear skin path from which maximal spike discharge activity could be evoked. Mean rate of spike firing evoked by each velocity (MFR) was computed for the time period during which spike discharge activity exceeded background, and an across-presentations estimate of mean firing rate (MFR) was generated for each velocity. The magnitude of the trial-by-trial variation in the response (estimated as CV; where CV = standard deviation in MFR/MFR) was determined for each unit at each velocity. MFR for both sMRAs and SI neurons (MFRsMRA and MFRSI, respectively) increased monotonically with velocity over the range 1-100 cm/s. At all velocities the average estimate of intertrial response variation for SI neurons (CVSI) was substantially larger than the corresponding average for sMRAs (CVsMRA). Whereas CVsMRA increased monotonically over the range 1-100 cm/s, CVSI decreased progressively with velocity over the range 1-10 cm/s, and then increased with velocity over the range 10-100 cm/s. The position of the skin brushing stimulus in the receptive field (RF) was varied in the second series of experiments. It was found that the magnitude of CVSI varied systematically with stimulus position in the RF: that is, CVSI was lowest for a particular velocity and direction of stimulus motion when the skin brushing stimulus traversed the RF center, and CVSI increased progressively as the distance between the stimulus path and the RF center increased. In the third series of experiments, either phencylidine (PCP; 100-500 microg/kg) or ketamine (KET; 0.5-7.5 mg/kg) was administered intravenously (iv) to assess the effect of block of N-methyl-D-aspartate (NMDA) receptors on SI neuron intertrial response variation. The effects of PCP on both CVSI and MFRSI were transient, typically with full recovery occurring in 1-2 h after drug injection. The effects of KET on CVSI and MFRSI were similar to those of PCP, but were shorter in duration (15-30 min). PCP and KET administration consistently was accompanied by a reduction of CVSI. The magnitude of the reduction of CVSI by PCP or KET was associated with the magnitude of CVSI before drug administration: that is, the larger the predrug CVSI, the larger the reduction in CVSI caused by PCP or KET. PCP and KET exerted variable effects on SI neuron mean firing rate that could differ greatly from one neuron to the next. The results are interpreted to indicate that SI neuron intertrial response variation is 1) stimulus tuned (intertrial response variation is lowest when the skin stimulus moves at 10 cm/s and traverses the neuron's RF center) and 2) NMDA receptor dependent (intertrial response variation is least when NMDA receptor activity contributes minimally to the response, and increases as the contribution of NMDA receptors to the response increases). (+info)Electromyographic assessment of neuromuscular block at the gastrocnemius muscle. (4/235)
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. (+info)Comparison of intubating conditions after rapacuronium (Org 9487) and succinylcholine following rapid sequence induction in adult patients. (5/235)
We have assessed intubating conditions provided by rapacuronium (Org 9487) and succinylcholine after rapid sequence induction of anaesthesia in adult patients undergoing elective surgery. We studied 335 patients, ASA I and II, in five centres. Two hundred and thirty-four subjects with normal body weight and 101 obese subjects were allocated randomly to one of four treatment groups differing in the neuromuscular blocking drug administered (rapacuronium 1.5 mg kg-1 or succinylcholine 1 mg kg-1) and in the technique used for induction of anaesthesia (fentanyl 2-3 micrograms kg-1 with thiopental 3-6 mg kg-1 or alfentanil 20 micrograms kg-1 with propofol 1.5-2 mg kg-1). Intubation was started at 50 s by an anaesthetist blinded to the drugs used. Intubating conditions were clinically acceptable (excellent or good) in 89.4% of patients after rapacuronium and in 97.4% after succinylcholine (P = 0.004), the estimated difference being 8.1% (95% confidence interval (CI) 2.0-14.1%). Neither anaesthetic technique nor subject group had an influence on intubating conditions. After intubation, the maximum increase in heart rate averaged 23.1 (SD 25.4%) and 9.4 (26.1%) after rapacuronium and succinylcholine, respectively (P < 0.001). Pulmonary side effects (bronchospasm and increased airway pressure) were observed in 10.7% (95% CI 5.8-17%) and 4.1% (95% CI 1.3-8.8%) of patients given rapacuronium and succinylcholine, respectively (P = 0.021). We conclude that after rapid sequence induction of anaesthesia in adults, clinically acceptable intubating conditions were achieved less frequently after rapacuronium 1.5 mg kg-1 than after succinylcholine. (+info)Rapid and reversible effects of activity on acetylcholine receptor density at the neuromuscular junction in vivo. (6/235)
Quantitative fluorescence imaging was used to study the regulation of acetylcholine receptor (AChR) number and density at neuromuscular junctions in living adult mice. At fully functional synapses, AChRs have a half-life of about 14 days. However, 2 hours after neurotransmission was blocked, the half-life of the AChRs was now less than a day; the rate was 25 times faster than before. Most of the lost receptors were not quickly replaced. Direct muscle stimulation or restoration of synaptic transmission inhibited this process. AChRs that were removed from nonfunctional synapses resided for hours in the perijunctional membrane before being locally internalized. Dispersed AChRs could also reaggregate at the junction once neurotransmission was restored. The rapid and reversible alterations in AChR density at the neuromuscular junction in vivo parallel changes thought to occur in the central nervous system at synapses undergoing potentiation and depression. (+info)Spontaneous or neostigmine-induced recovery after maintenance of neuromuscular block with Org 9487 (rapacuronium) or rocuronium following an initial dose of Org 9487. (7/235)
We have examined spontaneous and neostigmine-induced recovery after an initial dose of Org 9487 1.5 mg kg-1 followed by three repeat doses of Org 9487, a 30-min infusion of Org 9487 or two incremental doses of rocuronium. Mean clinical duration after incremental doses of Org 9487 0.5 mg kg-1 increased from 12.3 (SD 3.4) min to 14.0 (4.0) and 15.9 (5.9) min (P < 0.01), and after rocuronium from 14.4 (5.2) min to 19.2 (5.9) min (P < 0.01). Times for spontaneous recovery from a T1 of 25% to a TOF ratio of 0.8 after the last bolus dose of Org 9487 and after a 30-min infusion were 72.4 (16.5) and 66.1 (26.9) min compared with 36.7 (15.8) min in the group receiving reocuronium. These times were significantly reduced to 9.9 (4.5), 8.6 (6.1) and 5.7 (2.5) min, respectively, after neostigmine administration at a T1 of 25% (P < 0.05). We conclude that administration of Org 9487 by repeat bolus doses or infusion was associated with slow spontaneous recovery but neostigmine administration resulted in adequate recovery in less than 10 min. (+info)Anaesthesia for strabismus surgery: a regional survey. (8/235)
An increase in the demand by local surgeons for neuromuscular block during strabismus surgery, and the forced duction test in particular, led us to review the literature and conduct a regional survey of anaesthetic techniques used. A questionnaire was distributed to 379 anaesthetists in the region and 264 responses were received. The results demonstrated that 55% of paediatric patients and 66% of adult patients may have been operated on under suboptimal conditions; residual tone may have been present in the extraocular muscles during forced duction testing and strabismus correction. (+info)Prevalence: Delayed emergence from anesthesia is not uncommon, occurring in up to 20% of all anesthesia cases. The risk of delayed emergence is higher in patients with pre-existing medical conditions, such as heart disease or obesity.
Causes: There are several possible causes of delayed emergence from anesthesia, including:
1. Difficulty in weaning the patient off the anesthetic drugs.
2. Respiratory depression or other respiratory complications.
3. Inadequate pain management.
4. Sepsis or other systemic infections.
5. Coagulopathy or bleeding disorders.
6. Pre-existing medical conditions, such as heart disease or obesity.
7. Medications taken before the procedure.
8. Poor patient positioning during the procedure.
9. Inadequate monitoring of vital signs.
10. Anesthesia technique and choice of anesthetic agents.
Signs and Symptoms: Delayed emergence from anesthesia can be characterized by a range of signs and symptoms, including:
1. Prolonged unresponsiveness to stimuli.
2. Slow return of consciousness.
3. Confusion or disorientation upon regaining consciousness.
4. Delirium or hallucinations.
5. Increased heart rate and blood pressure.
6. Decreased respiratory rate.
7. Blue tinge to the skin (cyanosis).
8. Abnormal liver function test results.
9. Elevated white blood cell count.
10. Low body temperature.
Diagnosis: The diagnosis of delayed emergence from anesthesia is based on a combination of clinical signs and symptoms, as well as laboratory tests and imaging studies. The anesthesiologist will perform a thorough physical examination and ask questions about the patient's medical history to identify any potential causes of the delayed emergence. Laboratory tests may be ordered to check for signs of infection or other complications, while imaging studies such as CT scans or MRI scans may be used to evaluate the brain for any structural abnormalities.
Treatment: Treatment of delayed emergence from anesthesia is aimed at addressing the underlying cause and supporting the patient until they fully recover. This may include:
1. Oxygen therapy to help maintain adequate oxygenation of the body's tissues.
2. Pain management medications to alleviate any discomfort or pain.
3. Antibiotics to treat any infections that may have developed.
4. Supportive care, such as fluid replacement and monitoring of vital signs.
5. In some cases, the anesthesiologist may choose to use a different type of anesthesia or sedative to help the patient emerge more quickly.
Prognosis: The prognosis for patients who experience delayed emergence from anesthesia is generally good, especially if the underlying cause can be identified and treated promptly. However, in some cases, delayed emergence may be a sign of a more serious complication, such as brain damage or infection, which can have long-term consequences.
Prevention: Preventing delayed emergence from anesthesia is not always possible, but there are steps that can be taken to minimize the risk. These include:
1. Using a balanced anesthesia plan that takes into account the patient's medical history and other factors.
2. Monitoring the patient closely during the procedure and immediately after recovery.
3. Ensuring that the patient is properly positioned and has adequate oxygenation and ventilation.
4. Avoiding over-sedation, which can increase the risk of delayed emergence.
5. Using appropriate doses of anesthesia and sedatives, and avoiding high doses whenever possible.
1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.
Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.
Respiratory alkalosis can occur due to various causes such as hypoventilation (breathing too slowly), hypercapnia (excessive carbon dioxide in the blood), bicarbonate therapy, or drinking excessive amounts of antacids. Symptoms may include vomiting, abdominal pain, headache, and muscle weakness.
Treatment typically involves addressing the underlying cause, such as correcting hypoventilation or removing excess carbon dioxide from the bloodstream. In severe cases, medications or mechanical ventilation may be necessary.
1. Infection: Bacterial or viral infections can develop after surgery, potentially leading to sepsis or organ failure.
2. Adhesions: Scar tissue can form during the healing process, which can cause bowel obstruction, chronic pain, or other complications.
3. Wound complications: Incisional hernias, wound dehiscence (separation of the wound edges), and wound infections can occur.
4. Respiratory problems: Pneumonia, respiratory failure, and atelectasis (collapsed lung) can develop after surgery, particularly in older adults or those with pre-existing respiratory conditions.
5. Cardiovascular complications: Myocardial infarction (heart attack), cardiac arrhythmias, and cardiac failure can occur after surgery, especially in high-risk patients.
6. Renal (kidney) problems: Acute kidney injury or chronic kidney disease can develop postoperatively, particularly in patients with pre-existing renal impairment.
7. Neurological complications: Stroke, seizures, and neuropraxia (nerve damage) can occur after surgery, especially in patients with pre-existing neurological conditions.
8. Pulmonary embolism: Blood clots can form in the legs or lungs after surgery, potentially causing pulmonary embolism.
9. Anesthesia-related complications: Respiratory and cardiac complications can occur during anesthesia, including respiratory and cardiac arrest.
10. delayed healing: Wound healing may be delayed or impaired after surgery, particularly in patients with pre-existing medical conditions.
It is important for patients to be aware of these potential complications and to discuss any concerns with their surgeon and healthcare team before undergoing surgery.
Clindamycin
Trevor M. Jones
Benzodiazepine withdrawal syndrome
Metocurine
Paramedic
Sugammadex
Candicine
Rapid sequence induction
Anesthesia awareness
Fazadinium bromide
Lateral pectoral nerve
Amikacin
Dantrolene
Mipartoxin-I
Neuromuscular monitoring
Cerebral edema
Capreomycin
Neuromuscular blocking agents
Malouetine
Neuromuscular junction disease
Cholinesterase
Anesthetic
Cyclophosphamide
Acceleromyograph
Edrophonium
History of general anesthesia
Huwentoxin
Neuromuscular junction
Neuromuscular-blocking drug
Vecuronium bromide
Enzyme inhibitor
Ball and chain inactivation
Epigenetics of neurodegenerative diseases
Β-Alanine
Total intravenous anaesthesia
Stellate ganglion
Stiff-person syndrome
Society of Intensive Care Medicine
Botulism
4-Aminopyridine
Spinal anaesthesia
Negative-pressure pulmonary edema
Malignant hyperthermia
Postoperative residual curarization
Notexin
Agatoxin
Epigenetics of autoimmune disorders
Brachial plexus block
Alcuronium chloride
Anesthesiology
Dibucaine number
Early Neuromuscular Blockade in the Acute Respiratory Distress Syndrome
DailyMed - Search Results for Neuromuscular Nondepolarizing Blockade
Quantitative Neuromuscular Monitor for Neuromuscular Blockade
DailyMed - Search Results for Neuromuscular Depolarizing Blockade
Episode 77: Reversal of Neuromuscular Blockade | ACCRAC Podcast
FDA Approves Sugammadex for Reversing Neuromuscular Blockade | NYSSOMS
Reversal from neuromuscular blockade | International Journal of Current Research
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The effect of neuromuscular blockade on the efficiency of mask ventilation of the lungs. - Oxford Neuroscience
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Reversal agent for neuromuscular2
- Schaller S, Fink H. Sugammadex as a reversal agent for neuromuscular block: an evidence-based review. (accrac.com)
- Galantamine has an extensive record of activity as a reversal agent for neuromuscular blockade. (nih.gov)
Blocking Agents3
- McLean DJ, Diaz-Gil D, Farhan HN, Ladha KS, Kurth T, Eikermann M. Dose-dependent Association between Intermediate-acting Neuromuscular-blocking Agents and Postoperative Respiratory Complications. (accrac.com)
- Should be administered only by individuals experienced in the use of neuromuscular blocking agents. (drugs.com)
- The intentional interruption of transmission at the NEUROMUSCULAR JUNCTION by external agents, usually neuromuscular blocking agents. (nih.gov)
Succinylcholine3
- Subsequent neuromuscular transmission is inhibited so long as adequate concentration of succinylcholine remains at the receptor site. (pediatriconcall.com)
- Chronically administered oral contraceptives, glucocorticoids, or certain Monoamine Oxidase Inhibitors: The neuromuscular blocking effect of succinylcholine may be enhanced by drugs that reduce plasma cholinesterase activity. (pediatriconcall.com)
- Rapid neuromuscular blockade: are there alternatives to succinylcholine? (wustl.edu)
Respiratory Distress3
- The benefits of early continuous neuromuscular blockade in patients with acute respiratory distress syndrome (ARDS) who are receiving mechanical ventilation remain unclear. (nih.gov)
- Neuromuscular blockade is associated with the attenuation of biomarkers of epithelial and endothelial injury in patients with moderate-to-severe acute respiratory distress syndrome. (nih.gov)
- BACKGROUND: Neuromuscular blockade (NMB) is a therapy for acute respiratory distress syndrome (ARDS). (nih.gov)
Antagonism2
- 2023 American Society of Anesthesiologists Practice Guidelines for Monitoring and Antagonism of Neuromuscular Blockade. (blinkdc.com)
- Reversal (Antagonism) of Neuromuscular Blockade. (accrac.com)
Sugammadex3
- Hristovska AM, Duch P, Allingstrup M, Afshari A. Efficacy and safety of sugammadex versus neostigmine in reversing neuromuscular blockade in adults. (accrac.com)
- Sugammadex: A Review of Neuromuscular Blockade Reversal. (accrac.com)
- 19. Efficacy and safety of sugammadex versus neostigmine in reversing neuromuscular blockade in adults. (nih.gov)
Depolarizing1
- Depolarizing neuromuscular blocking agent. (drugs.com)
Anesthesia1
- Neuromuscular blockade is commonly used to produce MUSCLE RELAXATION as an adjunct to anesthesia during surgery and other medical procedures. (nih.gov)
Intraoperative1
- Careful intraoperative management of neuromuscular blockade may optimize patient recovery and improve postoperative outcomes. (apsf.org)
Onset2
- In regards to deciding which anti-cholinergic to match with which anti-cholinesterase to reverse neuromuscular blocking drugs, you specifically mention onset of action -atropine with edrophonium / glycopyrrolate with neostigmine. (accrac.com)
- because of its rapid onset and short duration of action, generally considered neuromuscular blocking agent of choice in emergency situations when rapid intubation (e.g., rapid sequence intubation) is required. (drugs.com)
Median1
- median dose, 1807 mg), and 86 of the 505 patients (17.0%) in the control group received a neuromuscular blocking agent (median dose, 38 mg). (nih.gov)
Assess1
- 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. (ox.ac.uk)
Monitoring2
- Recommended by ASA Neuromuscular Monitoring Guidelines. (blinkdc.com)
- Quantitative train of four (TOF) monitoring eliminates the guesswork in the assessment of neuromuscular block. (blinkdc.com)
Vecuronium1
- Merck Sharp and Dohme Corp.) to reverse the effects of the neuromuscular blocking drugs rocuronium bromide and vecuronium bromide. (nyssoms.org)
Continuous1
- careful assessment with a peripheral nerve stimulator is recommended during continuous IV infusions to monitor the degree of neuromuscular blockade, to detect the development of phase II block, and to minimize the possibility of overdosage. (drugs.com)
Block1
- It is distinguished from NERVE BLOCK in which nerve conduction ( NEURAL CONDUCTION ) is interrupted rather than neuromuscular transmission. (nih.gov)
Agent1
- Galantamine is a useful agent for the treatment of Alzheimer disease and for the reversal of neuromuscular blockade. (nih.gov)
Failure1
- The failure of neuromuscular transmission as a result of pathological processes is not included here. (nih.gov)
Effects2
- MRI measurement of the effects of moderate and deep neuromuscular blockade on the abdominal working space during laparoscopic surgery, a clinical study. (bvsalud.org)
- Conflicting data exist regarding the effects of deep neuromuscular blockade (NMB) on abdominal dimensions during laparoscopic procedures . (bvsalud.org)
Drugs1
- Appiah-Ankam J, Hunter J. Pharmacology of neuromuscular blocking drugs. (accrac.com)
Drug1
- 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. (ox.ac.uk)
Patients2
- 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. (ox.ac.uk)
- We conclude that neuromuscular blockade does not affect the efficiency of mask ventilation in patients with normal airways. (ox.ac.uk)
Study1
- We performed a clinical study to establish the influence of moderate and deep neuromuscular blockade (NMB) on the abdominal working space, measured by Magnetic Resonance Imaging (MRI), during laparoscopic donor nephrectomy with standard pressure (12 mmHg) pneumoperitoneum under sevoflurane anaesthesia. (bvsalud.org)