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Results for “Neuromuscular Blockade”

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PubMed1989

Spontaneous recovery of residual neuromuscular blockade after atracurium or vecuronium during isoflurane anaesthesia.

With atracurium and vecuronium, spontaneous recovery of residual neuromuscular blockade monitored electromyographically during 0.5% isoflurane anaesthesia was studied in 60 patients undergoing plastic surgery. After thiopentone, in random order, either atracurium 0.5 mg kg-1 or vecuronium 0.1 mg kg-1 was administered and isoflurane added to N2O and O2 mixture. Following spontaneous recovery of both the single twitch amplitude (T1) to 75% of the control value and the train-of-four ratio (TOF ratio) to 75%, incremental doses of the relaxant were given to maintain the T1 at less than 10%. Before the end of surgery, the blockade was again permitted to recover spontaneously. During the initial spontaneous recovery, the mean recovery time of T1 from 25% to 75% (the recovery index) with atracurium was longer (P less than 0.001) than that with vecuronium (13.2 min and 10.1 min, respectively) but, during the second recovery, the mean recovery index was shorter (P less than 0.05) with atracurium than with vecuronium (16.1 min and 19.8 min, respectively). The recovery time from T1 75% to TOF ratio 75%, indicating the recovery rate of residual neuromuscular blockade, with atracurium was about 15 min after both the initial and the second recoveries. With vecuronium, the respective recovery times were significantly (P less than 0.001) longer (25.6 min and 38.5 min, respectively). It is concluded that with vecuronium there is slower spontaneous recovery of residual neuromuscular blockade than with atracurium.

Adult↗

PubMed1996

[Caffeine antagonizes the neuromuscular blockade of vecuronium].

It is known that theophylline antagonizes the neuromuscular blockade in animals and case reports, where the same phenomenon has been observed in man, are described. One patient is described where another methylxantine-caffeine-caused resistance to neuromuscular blockade by vecuronium, but successful blockade was achieved by pancuronium.

Adult↗

PubMed1988

Clinical assessment of neuromuscular blockade produced by vecuronium using twitch, train of four, tetanus and post-tetanic twitch responses of the adductor pollicis muscle.

In the present investigation, the phenomenon of post-tetanic twitch potentiation (PTP) has been used to provide a sensitive index for neuromuscular blockade during an intense paralysis of the adductor pollicis muscle in man. We have also used and compared PTP assessment with that of twitch, train of four and tetanus in the same muscle and in the absence and presence of vecuronium (50 micrograms.kg-1). Vecuronium had a rapid onset of blockade (5-10s) and an intermediate duration of action (22-26 min). During the onset of blockade, the PTP response was still remaining (residual) whereas all the other mechanical responses disappeared within 2.5 min (Fig. 1b, c, d). Thus, the PTP values increased (upto 300% of control value of 18%, Fig. 1a) with increasing the intensity of neuromuscular blockade. The PTP value provided a better index for assessing the degree of neuromuscular blockade than did the twitch, train of four or the tetanus. However, during the onset of blockade, the PTP technique can also delay the onset of blockade, i.e. it has a decurarizing effect (Fig. 1b, c, d). During recovery of neuromuscular blockade, the PTP is actively involved in the enhancement of spontaneous recovery process, i.e. enhancement of de-curarization with repetitive stimulation of the ulnar nerve. In this respect, the PTP response recovers first, followed by the tetanus, train of four and the twitch responses. Thus the latter may be considered as a more sensitive index for the recovery process.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Effect of ketorolac tromethamine on atracurium-induced neuromuscular blockade in anesthetized dogs.

OBJECTIVE: The purpose of this study was to determine the effect of ketorolac tromethamine or placebo on the neuromuscular blockade induced by an infusion of atracurium in isoflurane-anesthetized dogs. DESIGN: Randomized, controlled trial. ANIMALS: Six healthy, adult mixed-breed dogs (five female, one male) weighing 24.8 +/- 2.8 kg. METHODS: Dogs were studied on two occasions with a minimum of 7 days between studies. Dogs were induced with 5% isoflurane in oxygen and maintained with 1.6 x minimum alveolar concentration (MAC) end-tidal isoflurane. Neuromuscular blockade was assessed using the train-of-four response. Once 50% depression of the first twitch (T1) was achieved, the atracurium infusion rate was held constant for 30 minutes. Then ketorolac, 0.5 mg/kg, or the same volume of placebo (0.9% sodium chloride solution) was administered intravenously and the atracurium infusion maintained for an additional 60 minutes. Before and at 2, 5, 10, 15, 30, and 60 minutes after ketorolac or placebo, the percent depression of T1 and the fourth twitch to the first twitch (T4/T1) ratio were recorded. The atracurium infusion was discontinued and the time for T1 to recover from 50% to 75% of its original value was recorded. At 75% T1, edrophonium, 0.5 mg/kg intravenously, was administered to antagonize the residual blockade. RESULTS: There was no significant difference in T1%, T4/T1 ratio, or recovery time after ketorolac administration compared with placebo. CONCLUSIONS: Ketorolac, 0.5 mg/kg intravenously, has no significant effect on either atracurium-induced neuromuscular blockade or recovery time for T1 in isoflurane-anesthetized dogs. CLINICAL RELEVANCE: The concurrent use of atracurium should not be a contraindication for the administration of ketorolac for intraoperative or postoperative analgesia.

Administration, Inhalation↗

PubMed2005

Acceleromyography in neonates and small infants: baseline calibration and recovery of the responses after neuromuscular blockade with rocuronium.

BACKGROUND: We have evaluated the use of the TOF-Guard (TOF, train-of-four) acceleromyographic thumb responses to ulnar nerve stimulation in neonates and infants and the return of the responses after neuromuscular blockade. METHODS: Baseline acceleromyographic recording of thumb adduction to ulnar nerve stimulation during volatile anaesthesia was performed in 22 babies aged less than 30 weeks. At the start of stimulation the automatic set-up procedure of the TOF-Guard was used to see if a 100% control twitch height could be achieved. Irrespective of the ability to achieve a 100% control twitch height, TOF stimulation was used thereafter. When no automatic 100% control twitch could be reached, the transducer signal gain factor was set manually to obtain a 100% value. In 14 of the 22 children the recovery after neuromuscular blockade with rocuronium 0.3 mg kg(-1) was recorded. RESULTS: In nine of 22 patients a 100% baseline twitch height was obtained with the automatic set-up. In the other 13 babies the TOF-Guard display indicated that the transducer signal was too low. The mean time to recovery of control twitch to 75% of baseline after rocuronium 0.3 mg kg(-1) was 51 min (SD = 21) and the time to recovery of the TOF ratio to 70% was 49 min (SD = 19). The mean final twitch height and TOF after recovery from rocuronium blockade were 101% (SD = 15) and 92% (SD = 12), respectively. CONCLUSION: The recovery of the responses after neuromuscular blockade to near baseline values shows that acceleromyography can be used to measure neuromuscular block and recovery in neonates and infants.

Androstanols↗

PubMed1995

[Potential of succinylcholine-induced neuromuscular blockade by nitrous oxide].

To evaluate the potentiating effect of nitrous oxide on the succinylcholine (SCh)-induced neuromuscular blockade, 0.16, 0.20, 0.25 or 0.31 mg.kg-1 of Sch was given during thiamylal-fentanyl anesthesia with or without nitrous oxide, and the evoked electromyograph of hypothenar muscles was measured. ED50 and ED95 in the group receiving nitrous oxide were 0.187 and 0.301 mg.kg-1, and 0.218 and 0.389 mg.kg-1 in the group not receiving nitrous oxide respectively. In the presence of nitrous oxide, the dose-response curve (DRC) was shifted to the left significantly (P < 0.01). By the multiple regression analysis, the degree of the neuromuscular blockade was shown to be affected by dose and nitrous oxide. It was demonstrated that nitrous oxide decreased electromyographically measured SCh requirements by 16.1%. In addition, the dose-effect relationship for SCh-induced neuromuscular blockade varied widely, and gender did not affect the degree of block.

Adolescent↗

PubMedDate not supplied

Circulatory responses and halothane concentrations during gastric or gallbladder traction with and without neuromuscular blockade.

Systolic and diastolic blood pressures and heart rates did not change significantly and ventricular dysrhythmias did not occur during gastric or gallbladder traction in patients anesthetized with N2O-halothane, with or without d-tubocurarine or pancuronium neuromuscular blockade. Systolic and diastolic blood pressures and heart rates just before abdominal viscera traction were less (p is less than 0.05) in patients paralyzed with d-tubocurarine than with pancuronium despite similar arterial halothane concentrations. In contrast, these measurements in patients without neuromuscular blockade were similar to those during pancuronium paralysis despite significantly greater arterial halothane concentrations in the unparalyzed patients. The authors conclude that circulatory responses during gastric or gallbladder traction are clinically insignificant during N2O-halothane administration, with or without d-tubocurarine or pancuronium neuromuscular blockade. Intraoperative blood pressures and heart rates were influenced by the neuromuscular blocker chosen. Neuromuscular blockade permitted anesthetic maintenance with lower arterial halothane concentrations than when paralysis was not present.

Abdomen↗

PubMed1987

Electrical and mechanical responses after neuromuscular blockade with vecuronium, and subsequent antagonism with neostigmine or edrophonium.

Six unpremedicated patients who had given their informed consent were given vecuronium 0.08 mg kg-1 before elective surgery. Recovery from neuromuscular blockade was measured electrically and mechanically. Neuromuscular blockade was antagonized 1 h after the administration of vecuronium with two doses of neostigmine 2.5 mg (three patients) or edrophonium 0.5 mg kg-1 (three patients). Although the onset of initial recovery was similar, subsequent recovery was faster when measured electrically (EMG) than when measured mechanically. Recovery appeared to be faster in younger patients. Reintroduction of neuromuscular blockade occurred after the second dose of neostigmine 2.5 mg, given to antagonize the block. This did not occur after either dose of edrophonium 0.5 mg kg-1.

Adult↗

PubMed2005

Control of neuromuscular blockade in the presence of sensor faults.

The problem of embedding sensor fault tolerance in feedback control of neuromuscular blockade is considered. For tackling interruptions of feedback measurements, a structure based upon Bayesian inference as well as a predictive filter is proposed. This algorithm is general and can be applied to different situations. Here, it is incorporated in an adaptive automatic system for feedback control of neuromuscular blockade using continuous infusion of muscle relaxants. A significant contribution consists in the experimental clinical testing of the algorithm in patients undergoing surgery.

Algorithms↗

PubMed1990

Effect of gentamicin administration on the neuromuscular blockade induced by atracurium in cats.

Atracurium besylate, a nondepolarizing neuromuscular blocking agent, was administered as an infusion to 8 anesthetized cats in which neuromuscular blockade was assessed, using the train-of-four response. Once 50% depression of the first-twitch (T1) response was achieved, the infusion was held constant for 60 minutes before being discontinued and the recovery time was determined. The time for recovery was recorded as the time for the train-of-four (T4 ratio) to increase from 50% to 75%. After recovery, atracurium infusion was reinstituted and the cats were again maintained for 60 minutes at 50% depression. A single bolus of gentamicin sulfate (2.0 mg/kg of body weight) was administered IV, and the infusion was continued for another 60 minutes before it was discontinued and the time for recovery was recorded. Within 1 minute of gentamicin administration, the mean +/- SD T1 response decreased from 49 +/- 5% to 33 +/- 8% of baseline and the T4 ratio decreased from 28 +/- 19% to 14 +/- 11%. Peak effect occurred at 5 minutes, with a T1 response of 29 +/- 6% of baseline and a T4 ratio of 13 +/- 12%. By 60 minutes after gentamicin administration, the T1 response had increased to 38 +/- 7% of baseline and the T4 ratio had increased to 21 +/- 13%. The time for recovery significantly (P less than 0.03) increased from 9.9 +/- 3.4 minutes during the control study to 18.1 +/- 10.7 minutes during the gentamicin study. In this study, gentamicin potentiated the neuromuscular blockade induced by atracurium and increased the recovery time. Residual blockade, observed after gentamicin administration was reversed with edrophonium.

Anesthesia↗

PubMed1988

Defining a region on tetanus toxin responsible for neuromuscular blockade.

Administering high doses of tetanus toxin to animals produces neuromuscular blockade. Previous studies, in which specific F(ab) antibody fragments were used to mask the 50,000 MW COOH-terminal portion of the heavy chain (fragment c) on the toxin molecule, have shown that the paralyzing effect of the toxin was most probably located in an area comprising the light chain and the 50,000 MW NH2-terminal portion of the heavy chain (Fragment Ibc). In our study, the toxin was also complexed with F(ab) fragments directed to the light chain (alpha), heavy chain (beta), beta minus IIc, and with monoclonal antibodies to epitopes on IIc and beta minus IIc. Investigating the effect of the resulting complexes both in mice and on the sphincter pupillae muscle in rabbits permitted us to circumscribe further the tetanus toxin neuromuscular blocking activity in a region of the NH2-terminal fragment (Mr = 50,000) of the heavy chain (fragment beta minus IIc). Our results are consistent with the assumption that the beta minus IIc fragment is critical for the neuromuscular blockade activity of tetanus toxin. However, it cannot be ruled out that both the peripheral and central effects of the toxin result from the same portion of the toxin molecule, the nature of the action depending on where the toxin is carried after its introduction into the organism.

Animals↗

PubMed1996

Economic impact of prolonged motor weakness complicating neuromuscular blockade in the intensive care unit.

OBJECTIVE: We compared a case-series of ten patients who developed prolonged neuromuscular weakness after continuous, nondepolarizing, neuromuscular blockade with a group of controls without neuromuscular weakness to determine the economic impact of the neuromuscular weakness. DESIGN: Frequency-matched case control trial. SETTING: Medical and surgical intensive care units of a 937-bed tertiary care, university-affiliated teaching hospital. PATIENTS: Ten patients developed prolonged neuromuscular weakness after continuous administration of nondepolarizing neuromuscular blockers. Ten patients from a 1994 drug utilization database who did not develop motor weakness after paralysis were identified to serve as controls. MEASUREMENTS AND MAIN RESULTS: The medical and accounting records of the patients were retrospectively reviewed. Charge data were obtained from patient accounts. Institutional ratios to convert charges to full costs and marginal costs were obtained from the Hospital Finance Department of Henry Ford Hospital. The economic impact of the diagnosis and recovery of the motor weakness was estimated for the intensive care unit (ICU) and hospital stays and compared with those values for control patients. Median hospital charges (excluding rehabilitation), totaling $91,476, were attributed to the patients who developed neuromuscular weakness and included charges for neuromuscular blocking agents, continuous mechanical ventilation, ICU and hospital beds, neurologic studies, and physical therapy services. In the control patients, median charges were $22,191 (p = .001). The total median cost differential for a patient in the neuromuscular weakness group was in excess of $66,713 (95% confidence interval $23,485 to $189,214, p = .001). Significant differences were also found for patient charges, full costs, and marginal costs for mechanical ventilation (p = .002), neurologic studies (p = .014), as well as ICU (p = .002) and hospital (p = .001) stays. CONCLUSIONS: The development of motor weakness was associated with an increase in ICU and hospital stays, continued mechanical ventilation, and disproportionate healthcare expenditures in excess of $66,000 per patient. A prospective evaluation of the true prevalence of neuromuscular weakness after neuromuscular blockade and of the costs to the healthcare system is needed.

Adult↗

PubMed1995

Post-tetanic burst count: a stimulating pattern for profound neuromuscular blockade.

The purpose of this study was to compare the pattern of recovery from vecuronium 0.07 mg.kg-1 induced neuromuscular blockade using post-tetanic burst count (PTBC)-(three short tetanic bursts of 0.2 msec duration every 20 msec given every second following a tetanus), and post-tetanic count (PTC)-(0.2 msec single twitch stimuli given every second following a tetanus) using an accelerometer in 60 adult patients during nitrous oxide-oxygen-isoflurane anaesthesia. In addition, the relationship among PTBC, PTC, and T1 (the 1st response in the train-of-four (TOF) stimulation) was examined to investigate whether the PTBC had an advantage over the PTC or TOF for evaluating intense neuromuscular blockade. The PTBC was greater than PTC during the 15-35 min after the administration of vecuronium (unpaired t test with Bonferroni's correction, P < 0.05). Time to the return of PTB response was shorter than that of PTT (17.7 +/- 3.2 vs 22.7 +/- 3.7 min, unpaired t test, P = 0.0005). Time from the return of PTB to that of T1 was longer than the time from the return of PTC to that of T1 (13.3 +/- 2.6 vs 9.2 +/- 2.8 min, unpaired t test, P = 0.0003). At the return of T1, PTBC was greater than PTC (14.3 +/- 6.9 vs 9.4 +/- 2.3, unpaired t test, P = 0.0153). These results suggest that, using PTBC, a more profound level of neuromuscular blockade can be evaluated than that using PTC.

Adult↗

PubMedDate not supplied

Cardiovascular effects of neuromuscular blockade during induced hypothermia.

Young lambs were used to study the effects of progressive cooling and rewarming on cardiovascular function during neuromuscular blockade induced by gallamine. Initially, it was shown that gallamine exerted no immediate, direct haemodynamic effect in normothermic or hypothermic lambs (cooled by 10 degrees C). By comparison with hypothermic controls, neuromuscular blockade was associated with increases in left ventricular (LV) max dP/dt (153%; P less than 0.02) as cooling progressed, and even greater increases (232%; P less than 0.001) during rewarming. It was concluded that these changes seem likely to represent enhanced myocardial contractility since preload did not closely follow LV max dP/dt (heart rate and mean aortic pressure fell gradually during cooling but values were restored in the rewarming phase). LV max dP/dt in lambs given gallamine only after cooling also showed a similar response during rewarming. Results of this study may have clinical relevance relating to the mechanical recovery of the hypothermic heart in patients receiving neuromuscular blockade during cardiac surgery, and they argue against using gallamine as such an agent.

Animals↗

PubMed1997

Neostigmine requirements for reversal of neuromuscular blockade following an infusion of mivacurium.

PURPOSE: To study the efficacy of neostigmine compared with placebo for the antagonism of neuromuscular blockade at the end of a mivacurium infusion, and to determine its optimal dose. METHODS: One hundred adult patients undergoing an elective surgical procedure received a standardized anaesthetic with 20-30 micrograms.kg-1 alfentanil, a propofol infusion and nitrous oxide. Muscle relaxation was maintained at 90-95% T1 depression with 0.2 mg.kg-1 mivacurium followed by an infusion. Neuromuscular blockade was measured with an integrated evoked electromyogram in response to train-of-four (TOF) stimuli at the ulnar nerve every 20 sec. Patients were randomized into four groups. At the end of surgery, the mivacurium infusion was stopped and patients received, immediately, in a double-blind manner, neostigmine (10, 20, or 40 micrograms.kg-1) or placebo according to a random number table. The T1 and TOF ratio were recorded until adequate recovery of neuromuscular function (TOF ratio > 0.70). During the reversal period, non-invasive blood pressure and heart rate were recorded every minute. The incidence of postoperative nausea and vomiting (PONV) was recorded in the recovery room. RESULTS: Data from 94 patients who completed the protocol were analysed. Compared with placebo, neostigmine 10 micrograms.kg-1 did not reduce the time to TOF > 0.70 (17.0 +/- 5.1 vs 14.6 +/- 4.2 min respectively). However the time was decreased with neostigmine 20 micrograms.kg-1 and 40 micrograms.kg-1 (P < 0.001), but with no difference between these last two groups (11.4 +/- 3.0 and 11.4 +/- 3.5 min respectively). Changes in systolic blood pressure and heart rate were not different between the four groups. Very few PONV events were observed in all groups (global incidence 7.4%). CONCLUSION: Recovery of neuromuscular blockade following a mivacurium infusion is accelerated by neostigmine. A dose of neostigmine 20 micrograms.kg-1 appears optimal with no further reduction in recovery time obtained from a larger dose.

Adult↗

PubMed1997

Presynaptic snake beta-neurotoxins produce tetanic fade and endplate potential run-down during neuromuscular blockade in mouse diaphragm.

The present study investigated the ability of a number of presynaptic snake neurotoxins (snake beta-neurotoxins) to produce nerve-evoked train-of-four fade, tetanic fade and endplate potential run-down during the development of neuromuscular blockade in the isolated mouse phrenic-hemidiaphragm nerve-muscle preparation. All the snake beta-neurotoxins tested, with the exception of notexin, produced train-of-four and tetanic fade of nerve-evoked isometric muscle contractions. Train-of-four fade was not present during the initial depressant or facilitatory phases of muscle tension produced by the snake beta-neurotoxins but developed progressively during the final depressant phase that precedes complete neuromuscular blockade. The 'non-neurotoxic' bovine pancreatic phospholipase A2 and the 'low-toxicity' phospholipase A2 from Naja naja atra venom failed to elicit train-of-four fade, indicating that the phospholipase activity of the snake beta-neurotoxins is not responsible for the development of fade. Intracellular recording of endplate potentials (EPPs) elicited by nerve-evoked trains of stimuli showed a progressive run-down in EPP amplitude during the train following incubation with all snake beta-neurotoxins except notexin. Again this run-down in EPP amplitude was confined to the final depressant phase of snake beta-neurotoxin action. However when EPP amplitude fell to near uniquantal levels (< 3 mV) the extent of toxin induced-fade was reduced. Unlike postjunctional snake alpha-neurotoxins, prejunctional snake beta-neurotoxins interfere with acetylcholine release at the neuromuscular junction during the development of neuromuscular blockade. This study provides further support for the hypothesis that fade in twitch and tetanic muscle tension is due to an underlying rundown in EPP amplitude resulting from a prejunctional alteration of transmitter release rather than a use-dependent block of postjunctional nicotinic receptors.

Animals↗

PubMed1990

Prolonged neuromuscular blockade and ventilatory failure after renal transplantation and cyclosporine.

In a retrospective one-year study, we documented respiratory failure or prolonged neuromuscular blockade in eight of 65 patients with chronic renal failure who had received either vecuronium (four of 29 patients) or atracurium (four of 36 patients) during anaesthesia for kidney transplantation. We reviewed the charts of the patients and recorded all aspects of medication and anaesthesia to try to determine whether there might be a single factor associated with this high incidence (12 per cent) of respiratory failure. Anaesthesia for all patients was induced with thiopentone, isoflurane, and N2O/O2. Tracheal intubation was facilitated with muscle relaxants in a single bolus of vecuronium, 0.07 to 0.1 mg.kg-1, or atracurium, 0.3 to 0.5 mg.kg-1. Additional doses were given according to neuromuscular activity, which was monitored visually by response to train-of-four and tetanic stimulation. Anaesthesia was maintained with fentanyl/isoflurane and N2O/O2. After induction of anaesthesia, each patient received methylprednisolone, cefazolin, mannitol infusion for 24 hr beginning at the start of renal artery anatomosis, and either azathioprine (n = 57) or cyclosporine (n = 8). Relaxation was evaluated toward the end of the operation by train-of-four stimulation. Neuromuscular blockade was reversed with edrophonium (0.75-1 mg.kg-1) or neostigmine (0.06-0.08 mg.kg-1). The eight patients with prolonged neuromuscular blockade received ventilatory support for one to three hours after operation. Respiratory failure was significantly more frequent in patients who received cyclosporine (P less than 0.05).

Adult↗

PubMed2002

Residual neuromuscular blockade in the immediate postoperative period.

Neuromuscular blocking agents are among the most potent and dangerous drugs administered in the course of a general anesthetic. Their residual actions can have profound effects on a patient's ability to adequately ventilate. Understanding the basics of their actions and the methods of monitoring the level of neuromuscular blockade will assist the PACU nurse in diagnosing the cause of postoperative muscle weakness and hypoventilation. This article will review the mechanisms of action and monitoring of neuromuscular blocking agents, as well as provide a basic overview of postoperative complications involving hypoventilation and motor weakness.

Algorithms↗