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PubMed1993

Onset of maximum neuromuscular block following succinylcholine or vecuronium in four age groups.

BACKGROUND: Increasing age appears to be associated with a slower onset of neuromuscular blockade, but such an effect has not been studied with the same doses of the same drugs across pediatric and adult age groups. METHODS: The authors measured the evoked compound action potential of the adductor pollicis muscle in response to 0.1-Hz stimulation of the ulnar nerve, during fentanyl-thiopental-oxygen anesthesia, in 160 patients aged 1-3 yr, 3-10 yr, 20-40 yr, or 60-80 yr. Subparalyzing doses of vecuronium (0.03 mg/kg) or succinylcholine (0.3 mg/kg), or paralyzing doses of vecuronium (0.1 mg/kg) or succinylcholine (1.0 mg/kg), were administered to ten patients in each age group. RESULTS: Onset time, defined as the time from injection to maximum depression of response with a subparalyzing dose or the time from injection to ablation of visible response with a paralyzing dose, varied with age in all groups (P < 0.001). For 0.3 mg/kg succinylcholine, it increased from 49 +/- 6 s in 1-3-yr-old patients, to 104 +/- 9 s in 60-80-yr-old patients (P < 0.00001). For 0.03 mg/kg vecuronium, onset time was 3.6-5.9 times longer than for succinylcholine, increasing from 219 +/- 15 s in 3-10-yr-old patients to 473 +/- 30 s in 60-80-yr-old patients (P < 0.00001 by linear regression). For paralyzing doses, succinylcholine 1.0 mg/kg had an onset time of 58 +/- 7 s and 95 +/- 7 s, in 1-3-yr-old and 60-80-yr-old patients, respectively (P < 0.001). For 0.1 mg/kg vecuronium, onset time varied between 125 +/- 19 s in 1-3-yr-old patients to 295 +/- 31 s in 60-80-yr-old patients (P < 0.00001), and was 2.1-3.3 times longer than 1 mg/kg succinylcholine. CONCLUSIONS: Increasing age is associated with slower onset for both succinylcholine and vecuronium. When equipotent, subparalyzing doses of succinylcholine and vecuronium are compared, onset time is 4.5 times as long with vecuronium.

Adult↗
PubMed1995

Plasma cholinesterase and abnormal reaction to succinylcholine: twenty years' experience with the Danish Cholinesterase Research Unit.

For more than 20 years, the Danish Cholinesterase Research Unit (DCRU) has collected information about patients showing an abnormal response to succinylcholine. The purpose of this study was, on the basis of the 20 years' experiences with the Unit, to evaluate our clinical findings in patients referred because of prolonged response following succinylcholine. Also, we wanted to evaluate the results of our prospective controlled studies of the effect of succinylcholine in patients with normal and abnormal plasma cholinesterase genotypes. An explanation for the apparent abnormal response to succinylcholine was found in 61.1% of the 1,247 patients referred to the Unit. Of the 1,247 patients, 28.5% were genotypically normal and 46.5% had an abnormal genotype. In the remaining 24.9% of the patients, the genotype could not be established. The time to sufficient recovery of neuromuscular function following succinylcholine 1.0-1.5 mg kg-1 was 15-30 min in patients heterozygous for one abnormal gene, 35-45 min in patients heterozygous for two abnormal genes and 90-180 min in patients homozygous for the atypical gene. Patients with two newly discovered genotypes (AK (5 patients) and AH (1 patient) showed slightly prolonged (20 min) and markedly prolonged (90 min) duration of action of succinylcholine, respectively. Our results indicate that it is a problem for many anaesthetists to correctly diagnose a prolonged response to succinylcholine. We therefore urge the anaesthetist always to use a peripheral nerve stimulator when faced with a case of apparent abnormal response to succinylcholine.

Apnea↗
PubMed1992

Tyraminelike action of succinylcholine in the isolated, blood-perfused canine atrium.

The mechanisms of succinylcholine-induced cardiac effects have not been fully elucidated. Accordingly, we studied the effects of succinylcholine on atrial rate and contractile force in the isolated canine atrium perfused with donor blood. The sinus node artery was perfused with heparinized blood from the common carotid artery of the donor dog at a constant pressure of 100 mm Hg. When succinylcholine in a dose range of 30-1000 micrograms was injected directly into the sinus node artery of the isolated atrium, increases in atrial rate and contractile force were observed in a dose-related manner. The atrial rate and contractile force were increased to 10.5% +/- 1.8% (mean +/- SEM) and 56.8% +/- 8.5% above the control values after the administration of 1000 micrograms of succinylcholine, respectively. After treatment with propranolol, the positive chronotropic and inotropic effects of succinylcholine and norepinephrine were significantly suppressed. Hexamethonium or tetrodotoxin pretreatment inhibited the cardiac effects of nicotine but did not modify the succinylcholine-induced cardiac effects. The succinylcholine-induced effects were significantly inhibited by treatment with imipramine, which also suppressed the tyramine-induced effects. We conclude that succinylcholine has cardioexcitatory properties mediated by release of catecholamine due to a tyraminelike action.

Animals↗
PubMed2004

The neuromuscular effects and tracheal intubation conditions after small doses of succinylcholine.

UNLABELLED: Succinylcholine 1.0 mg/kg usually produces excellent tracheal intubation conditions in 60 s. Recovery of respiratory muscle function after this dose, however, is not fast enough to forestall oxyhemoglobin desaturation when ventilation cannot be assisted. In this study, we investigated whether smaller doses of succinylcholine can produce satisfactory intubation conditions fast enough to allow rapid sequence induction with a shorter recovery time. Anesthesia was induced with fentanyl/propofol and maintained by propofol infusion and N(2)O in O(2). After the induction, 115 patients were randomly allocated to five groups according to the dose of succinylcholine (0.3 mg/kg, 0.4 mg/kg, 0.5 mg/kg, 0.6 mg/kg, or 1.0 mg/kg). Evoked adductor pollicis responses to continuous 1-Hz supramaximal ulnar nerve stimulation were recorded using acceleromyography. Tracheal intubation conditions were graded 60 s after succinylcholine administration. Onset time, maximal twitch depression, time to initial twitch detection after paralysis, and to 10%, 25%, 50%, and 90% twitch height recovery were recorded. Time to initial diaphragmatic movement as well as time to resumption of regular spontaneous respiratory movements were calculated. Onset times ranged between 82 s and 52 s, decreasing with increasing doses of succinylcholine but not differing between 0.6 and 1 mg/kg. Maximum twitch depression was similar after 0.5, 0.6, and 1 mg/kg (98.2%-100%). Recoveries of twitch height and apnea time were dose-dependent. Intubation conditions were often unacceptable after 0.3- and 0.4-mg/kg doses. Acceptable intubation conditions were achieved in all patients receiving a 0.5, 0.6, and 1 mg/kg dose of succinylcholine. Intubation conditions in patients receiving 0.6 and 1 mg/kg were identical, whereas times to T(1) = 50% and 90% and time to regular spontaneous reservoir bag movements were significantly shorter in the 0.6-mg/kg dose group (5.78, 7.25, and 4.0 min, respectively) versus patients receiving 1 mg/kg (8.55, 10.54, and 6.16 min, respectively). The use of 0.5 to 0.6 mg/kg of succinylcholine can produce acceptable intubation conditions 60 s after administration. The conditions achieved after 0.6 mg/kg are similar to those after 1.0 mg/kg. These smaller doses are associated with faster twitch recovery and shorter apnea time. IMPLICATIONS: In normal healthy patients, succinylcholine 0.6 mg/kg produces clinical intubation conditions identical to the traditional 1.0-mg/kg dose but is associated with a shorter recovery time.

Adult↗
PubMed2004

Posttetanic potentiation and fade in the response to tetanic and train-of-four stimulation during succinylcholine-induced block.

UNLABELLED: We designed this study to confirm anecdotal observations that neuromuscular block after a single administration of succinylcholine is characterized by fade to train-of-four (TOF) or tetanic stimulation, as well as posttetanic potentiation. This prospective, randomized, 2-center observational study involved 100 patients. Patients were allocated to 1 of 5 groups and received 0.1, 0.3, 0.5, 0.75, or 1.0 mg/kg succinylcholine during propofol/fentanyl/nitrous oxide anesthesia. Neuromuscular function was monitored by TOF using mechanomyography. At 10%-20% spontaneous recovery of the first twitch of TOF, the mode of stimulation was changed from TOF to 1-Hz single-twitch stimulation followed by a tetanic stimulus (50 Hz) for 5 s. Three seconds later, the single twitch (1 Hz) was applied again for approximately 30 s followed by TOF stimulation until full recovery of the TOF response. Succinylcholine-induced neuromuscular block had the following characteristics: 1) twitch augmentation before twitch depression, which was seen more frequently in patients given smaller doses (0.1 and 0.3 mg/kg) than in those given larger doses (0.5-1.0 mg/kg); 2) TOF fade during onset and recovery of the block; 3) tetanic fade; and 4) and posttetanic potentiation. Posttetanic potentiation was related to the pretetanic twitch height but was not related to the dose of succinylcholine administered. Some characteristics of Phase II block were detectable during onset and recovery from doses of succinylcholine as small as 0.30 mg/kg. Posttetanic potentiation and fade in response to train-of-four and tetanic stimuli are characteristics of neuromuscular block after bolus administration of different doses of succinylcholine. IMPLICATIONS: Posttetanic potentiation and fade in response to train-of-four and tetanic stimuli are characteristics of neuromuscular block after bolus administration of different doses of succinylcholine. We also conclude that some characteristics of a Phase II block are evident from an initial dose (i.e., as small as 0.3 mg/kg) of succinylcholine.

Adult↗
PubMed2006

The dose of succinylcholine required for excellent endotracheal intubating conditions.

In this prospective, randomized, double-blind, placebo-controlled study, we attempted to define the dose of succinylcholine that provides excellent intubation conditions in patients within 60 s during simulated rapid-sequence induction of anesthesia. Anesthesia was induced in 180 patients with 2 microg/kg fentanyl and 2 mg/kg propofol. After loss of consciousness, patients were randomly allocated to receive 0.3, 0.5, 1.0, 1.5, or 2.0 mg/kg succinylcholine or saline solution (control group). Tracheal intubation was performed 60 s later. A blinded investigator performed all laryngoscopies and graded intubating conditions. Intubating conditions were excellent in 0.0%, 43.3%, 60.0%, 63.3%, 80.0%, and 86.7% of patients after 0.0, 0.3, 0.5, 1.0, 1.5, and 2.0 mg/kg succinylcholine, respectively. The incidence of excellent intubating conditions was significantly more frequent (P < 0.001) in patients receiving succinylcholine than in the controls and in patients who received 2.0 mg/kg succinylcholine (P < 0.05) than in those who received 0.3 mg/kg succinylcholine. The calculated doses of succinylcholine (and their 95% confidence intervals) that are required to achieve excellent intubating conditions in 50% and 80% of patients at 60 s are 0.39 (0.29-0.51) mg/kg and 1.6 (1.2-2.0) mg/kg, respectively. It appears that there are no advantages to using doses of succinylcholine larger than 1.5 mg/kg.

Adult↗
PubMed1993

Sustained focal effects of low-dose intramuscular succinylcholine.

We studied low-dose intramuscular succinylcholine in 9 subjects as part as an ongoing investigation of its potential to predict responses to botulinum toxin. We measured compound muscle action potentials (CMAPs) from the extensor digitorum brevis (EDB) muscles in each foot before and after intramuscular injections of 2.5 mg of succinylcholine into the EDB. Succinylcholine reduced mean CMAP amplitudes to 42% of baseline; the maximal reduction occurred at 19 +/- 6 (mean +/- standard deviation) minutes. Recovery to 73% of the baseline CMAP amplitude (approximately 50% recovery from block) occurred at 105 +/- 49 minutes after injection. Repetitive (train-of-four) stimulation at 2 Hz produced mild CMAP decrements (5-25%), but only during the recovery phase. Varying the succinylcholine concentrations (10, 20, or 50 mg/mL) while holding the total drug dose constant did not change the rate of onset or the extent of block. No systemic complications occurred. We conclude that: (1) 2.5 mg intramuscular succinylcholine can safely induce selective muscle weakness with a time course that differs from intravenously administered succinylcholine; and (2) further clinical studies comparing intramuscular succinylcholine and botulinum toxin are warranted.

Action Potentials↗
PubMed1986

Succinylcholine, fasciculations and myoglobinaemia.

The prophylactic effectiveness of a small "self-taming" dose of succinylcholine (0.1 mg X kg-1), of d-tubocurarine (0.05 mg X kg-1), and of pancuronium (0.02 mg X kg-1) on succinylcholine-induced fasciculations and myoglobinaemia was studied in 64 healthy children (ages two to nine years), anaesthetized with halothane, nitrous oxide and oxygen. Serum myoglobin was analyzed by radioimmunoassay and taken as a tracer of muscle damage. No correlation was found between the serum levels of myoglobin and the incidence of muscle fasciculations. Self-taming with succinylcholine decreased the incidence of fasciculations (p = 0.001) but did not decrease the succinylcholine-induced myoglobinaemia (p = 0.224). D-tubocurarine (0.05 mg X kg-1) and pancuronium (0.02 mg X kg-1) both significantly reduced the myoglobinaemia and the fasciculations produced by succinylcholine. The pancuronium pretreated group presented less variable values of serum myoglobin which, when compared to the control group, had a more significant p value (p less than 0.001) than for d-tubocurarine pretreated group (p = 0.003). Muscle fasciculations and increased myoglobin levels were observed in children less than four years old who received succinylcholine. The prophylaxis of acute rhabdomyolytic renal failure due to succinylcholine (seven cases reported in the medical literature) is considered.

Age Factors↗
PubMed1989

Ketamine enhances phase I and phase II neuromuscular block of succinylcholine.

The effect of intravenous injection of ketamine 2, 5 and 10 mg.kg-1 on the neuromuscular blocking action of succinylcholine was studied on the indirectly stimulated adductor pollicis muscle twitch of monkeys anaesthetized with 0.5-1.0 per cent halothane in oxygen. Neuromuscular block was quantified by single twitches evoked at 0.1 Hz. The changing nature of neuromuscular block from Phase I to Phase II was monitored periodically by train-of-four fade. In the absence of succinylcholine, ketamine had no consistent neuromuscular effect of its own. In the presence of succinylcholine, ketamine in a dose-dependent manner potentiated both the Phase I and the Phase II neuromuscular blocking effect of succinylcholine. In Phase I, 2 mg.kg-1 of ketamine reduced the ED50 of succinylcholine from 0.46 +/- 0.07 mg.kg-1 to 0.33 +/- 0.06 mg.kg-1 (P less than 0.01), and increased its 25-75 per cent recovery index from 4.0 +/- 0.4 min to 5.3 +/- 0.1 min (P less than 0.01). In Phase II, ketamine in the same dose deepened a steady neuromuscular block maintained by succinylcholine infusion from 48 +/- 3 per cent block to 71 +/- 2 per cent block (P less than 0.01). We concluded that ketamine potentiates the Phase I and the Phase II neuromuscular blocks of succinylcholine.

Anesthesia, Inhalation↗
PubMed2005

Recovery from paralysis with succinylcholine increased Response entropy and EMG but not State entropy.

OBJECTIVE: It is reported that the electromyogram is an indicator of patient arousal during pain stimulation if anesthesia is inadequate. This may not be true during recovery from succinylcholine induced paralysis. We evaluated State entropy of the electroencephalogram (EEG, 0.8-32 Hz) and Response entropy, a combined measure of the electromyogram (EMG) and EEG (0.8-47 Hz), during recovery from paralysis with succinylcholine. METHODS: Twenty patients were randomized to receive either 0.8% (n = 10) or 1.4% isoflurane (n = 10), with 2 mg/kg succinylcholine administered for paralysis in all patients. State entropy and Response entropy were evaluated using a Datex-Ohmeda Entropy module. Frontal EMG was measured separately by an EEG module. State entropy, Response entropy, and EMG were measured in awake patients, during isoflurane anesthesia and paralysis, and after 100% recovery to train of four stimulation. RESULTS: Response entropy and State entropy decreased from awake levels in a dose related manner during 0.8% or 1.4% isoflurane and succinylcholine. Recovery from succinylcholine significantly increased Response entropy and EMG in 5 of 10 patients with 0.8% isoflurane and 8 of 10 with 1.4% isoflurane without a change in State entropy. CONCLUSION: Although RE and EMG increased during recovery from paralysis with succinylcholine, SE, an indicator of EEG, was not stimulated. EMG activity may not be an indicator of patient arousal after succinylcholine treatment.

Anesthetics, Inhalation↗
PubMed1995

Interaction between mivacurium and succinylcholine.

We investigated the interaction between mivacurium and succinylcholine when mivacurium was administered during the early recovery from succinylcholine block. We studied 40 adult patients during propofol-alfentanil-N2O-O2 anesthesia. Neuromuscular function was monitored using an electromyographic method (Relaxograph, Datex, Helsinki, Finland). Patients randomly received either 1.0 mg/kg of succinyl-choline followed by 0.15 mg/kg of mivacurium when the first twitch (T1) during succinylcholine block recovered to 5%, or 0.15 mg/kg of mivacurium without succinylcholine. Serum cholinesterase activity was lower than normal range in two patients and higher than normal range in four patients, but the dibucaine number value was normal in every patient. The mean onset time (3.8 +/- 0.9 min) (mean +/- SD) or maximal neuromuscular block (96.6% +/- 7.2%) of mivacurium did not differ between the groups. The T1 recovery times of mivacurium were slightly shorter (P < 0.05) after succinylcholine administration than without it. During recovery of mivacurium block, the fade was significantly greater, i.e., the train-of-four (TOF) ratio was lower, after succinylcholine administration than without it. Recovery index (T1 25%-75%, mean 4.7 +/- 1.3 min) and the time from the administration of mivacurium to the recovery of TOF ratio 0.7 (mean 20.4 +/- 5.1 min) were not different between the groups. In conclusion, in healthy patients succinylcholine has negligible effects on a subsequent mivacurium-induced neuromuscular block.

Adolescent↗
PubMed1996

Comparison of rocuronium and mivacurium to succinylcholine during outpatient laparoscopic surgery.

Tracheal intubating conditions and neuromuscular effects of succinylcholine, rocuronium, and mivacurium were studied in 100 healthy women undergoing outpatient laparoscopic surgery. After a standardized fentanyl-thiopental induction, tracheal intubation was facilitated with succinylcholine 1 mg/kg in Groups I (n = 23) and II (n = 25), rocuronium 0.6 mg/kg in Group III (n = 27), or mivacurium 0.2 mg/kg in Group IV (n = 25). If clinically indicated, bolus doses of rocuronium 5-10 mg (Groups I and III) or mivacurium 2-4 mg (Groups II and IV) were administered during the maintenance period. Anesthesia was maintained with desflurane and nitrous oxide 60% in oxygen. At the end of the surgery, residual neuromuscular block was reversed with edrophonium 0.5 mg/kg and atropine 10 micrograms/kg, if needed. The neuromuscular function was assessed using electromyography with a train-of-four mode of stimulation every 10 s at the wrist. Intubating conditions 90 s after succinylcholine and rocuronium were significantly better than after mivacurium. The onset time (from the end of injection until 95% suppression of the first twitch [T1]) for succinylcholine (63 +/- 21 s and 62 +/- 17 s in Groups I and II, respectively) were significantly shorter than for rocuronium (158 +/- 76 s) or mivacurium (210 +/- 93 s). Moreover, the onset times for rocuronium were significantly shorter than mivacurium. The recovery times (of T1 to 25% of the control value) were significantly shorter with succinylcholine and mivacurium than rocuronium. Significantly fewer patients needed reversal of residual neuromuscular blockade after mivacurium compared to rocuronium. One patient in Group I and six patients in Group IV displayed erythema on the upper body. Postoperative myalgia were experienced by 16% of the patients in Groups I and II compared to none in Groups III and IV. There was on difference in the incidence of postoperative nausea and vomiting among the four groups. In conclusion, rocuronium appears to be an acceptable alternative to succinylcholine for tracheal intubation. However, rocuronium's longer duration of action increases the need for reversal drugs. When rapid tracheal intubation is unnecessary, mivacurium is also an acceptable alternative to succinylcholine and is associated with a more rapid spontaneous recovery than rocuronium.

Adult↗
PubMed1981

Mechanism of tracheal constriction by succinylcholine.

The purpose of this study was to identify the mechanism by which succinylcholine produced large increases in endotracheal tube cuff pressure in barbiturate-anesthetized dogs (n = 7). Cuff pressure was measured in vivo by a transducer connected to a fluidfilled, high-volume, low-pressure cuff. Intravenous succinylcholine, 0.5 and 1 mg/kg, produced mean increases in cuff pressure of 12 +/- 2 (+/-SE) and 27 +/- 5 cm H2O, respectively, which reached peak effect in 1 to 3 min and declined slowly over the next 10 min. Bilateral vagotomy, intravenous administration of atropine (0.2 mg/kg) and hexamethonium (5 mg/kg) prevented or terminated succinylcholine-induced increases in cuff pressure. Isolated preparations from an additional three dogs were employed to study the direct actions of succinylcholine on trachealis muscle in vitro. In organ baths, succinylcholine (10(-6) to 10(-3) M) did not contract canine trachealis muscle, and concentrations of 10(-5) M and above significantly relaxed carbamylcholine-induced contractions. The authors conclude that succinylcholine elicits contraction of trachealis muscle by a stimulant action on parasympathetic pathways rather than by a direct action on airway smooth muscle. Since vagotomy prevented the succinylcholine response, the site of stimulant action is not at autonomic ganglia.

Animals↗
PubMed1990

Paraben preservatives but not succinylcholine are cerebral vasodilators in vitro.

Since the increase in intracranial pressure produced by succinylcholine is temporally associated with intravenous administration, we investigated in vitro a possible direct cerebrovascular effect of this nicotinic drug. Isometric responses were recorded from dog and guinea pig basilar artery rings suspended in modified Krebs' solution at 37 degrees C. After precontracting with a voltage (KCl)- or a receptor (5-hydroxytryptamine)-mediated agonist, cumulative concentration-relaxation curves were established for: pure succinylcholine; Quelicin from multidose vials containing 20 mg/ml succinylcholine, 1.8 mg/ml methylparaben, and 0.2 mg/ml propylparaben; Anectine from single-dose vials containing 20 mg/ml succinylcholine; multidose Anectine containing 20 mg/ml succinylcholine and 1.0 mg/ml methylparaben; and methylparaben and propylparaben alone. When required, the endothelium of dog artery was removed by gentle mechanical rubbing and the response to the drugs reevaluated. Both Quelicin and multidose Anectine produced statistically significant (P less than 0.05) relaxation; Quelicin was the more potent of the two. Methylparaben and propylparaben produced relaxation in an additive manner and completely accounted for the relaxation produced by Quelicin and multidose Anectine. The vascular relaxation was found to be independent of the presence of a functional endothelium. Consistent with a nicotinic induced contraction, pure succinylcholine maintained vessel tone. It is concluded that the pharmaceutically ubiquitous preservatives methylparaben and propylparaben but not pure succinylcholine have vasoactive properties in vitro.

Animals↗
PubMed1999

Comparison of the intubation conditions provided by rapacuronium (ORG 9487) or succinylcholine in humans during anesthesia with fentanyl and propofol.

BACKGROUND: Currently, the only approved muscle relaxant with a rapid onset and short duration of action is succinylcholine, a drug with some undesirable effects. Rapacuronium is an investigational nondepolarizing relaxant that also has a rapid onset and short duration and consequently should be compared with succinylcholine in its ability to facilitate rapid tracheal intubation. METHODS: This prospective, randomized clinical trial involved 336 patients. Anesthesia was induced with fentanyl and propofol and either 1.5 mg/kg rapacuronium or 1.0 mg/kg succinylcholine. The goal was to accomplish tracheal intubation by 60 s after administration of the neuromuscular blocking drug. Endotracheal intubation was performed, and conditions were graded by a blinded investigator. Recovery of neuromuscular function was assessed by electromyography. RESULTS: Intubation conditions were evaluated in 236 patients. Intubation by 60 s after drug administration occurred in 100% of patients with rapacuronium and in 98% with succinylcholine. Intubation conditions were excellent or good in 87% of patients with rapacuronium and in 95% with succinylcholine (P < 0.05). The time (median and range) to the first recovery of the train-of-four response was 8.0 (2.8-20.0) min with rapacuronium and 5.7 (1.8-17.7) min with succinylcholine (P < 0.05). The overall incidence of adverse effects was similar with both drugs. CONCLUSIONS: A 1.5-mg/kg dose of rapacuronium effectively facilitates rapid tracheal intubation. It can be considered a valid alternative to 1.0 mg/kg succinylcholine for this purpose.

Adolescent↗
PubMed2005

Succinylcholine dosage and apnea-induced hemoglobin desaturation in patients.

BACKGROUND: The authors examined the notion that a reduction in succinylcholine dose from 1 mg/kg to approximately 0.6 mg/kg would allow a faster recovery of spontaneous ventilation and reduction in the incidence of hemoglobin desaturation during the period of apnea in simulated complete upper airway obstruction situations. METHODS: This prospective, randomized, double-blind study involved 60 patients. After preoxygenation to an end-tidal oxygen concentration >90%, patients were anesthetized with 2 microg/kg fentanyl and 2 mg/kg propofol. After loss of consciousness, patients were randomly allocated to receive 0.56 or 1.0 mg/kg succinylcholine or saline (control group). Oxygen saturation was monitored continuously at the index finger. When the patient became apneic, the face mask was removed and the patient's airway was left unsupported. If the oxygen saturation decreased to 90%, the face mask was reapplied, and ventilation was assisted until the patient was awake. Time from injection of the study drug to the first visible spontaneous diaphragmatic movements was noted. RESULTS: Oxygen saturation decreased <90% in 45%, 65%, and 85% of patients in the control, 0.56 mg/kg, and 1.0 mg/kg succinylcholine groups, respectively (P = 0.03). Corresponding times (mean +/- SD) to spontaneous of diaphragmatic movements were 2.7 +/- 1.2, 4.8 +/- 2.5, and 4.7 +/- 1.3 min, respectively. These times were longer (P < 0.001) after either dose of succinylcholine compared with controls. CONCLUSIONS: Reduction in succinylcholine dose from 1.0 mg/kg to 0.56 mg/kg decreased the incidence of hemoglobin saturation <90% from 85% to 65% but did not shorten the time to spontaneous diaphragmatic movements. A significant fraction of patients would be at risk if there were failure to intubate and ventilate whether succinylcholine is administered or not and regardless of the dose of succinylcholine administered.

Adult↗
PubMed1991

Pretreatment with d-tubocurarine, vecuronium, and pancuronium attenuates succinylcholine-induced increases in plasma norepinephrine concentrations in humans.

We studied in patients the effect of d-tubocurarine, which has sympathetic ganglion blocking action, on succinylcholine-induced increases in plasma levels of catecholamines, and compared it with the effects of vecuronium and pancuronium, which have little sympathetic ganglion blocking action. Thirty-two patients were divided into five groups: seven were given 3 mL saline; seven received 1 mg/kg succinylcholine; and six, seven, and five patients were given 0.08 mg/kg d-tubocurarine, 0.01 mg/kg vecuronium, and 0.01 mg/kg pancuronium, respectively, all of which were injected 5 min before 1 mg/kg succinylcholine. Succinylcholine alone significantly increased plasma norepinephrine concentrations, systolic blood pressure, and heart rate from 187 +/- 39 pg/mL (mean +/- SEM), 93 +/- 2 mm Hg, and 77 +/- 4 beats/min to 429 +/- 61 pg/mL, 120 +/- 7 mm Hg, and 102 +/- 6 beats/min, respectively, with onset of fasciculations. Pretreatment with d-tubocurarine, vecuronium, and pancuronium significantly and equally attenuated both the fasciculations and the cardiovascular responses to succinylcholine. These results suggest that the sympathetic ganglion blocking action of neuromuscular relaxants when given before succinylcholine is not an important factor in attenuation of succinylcholine-induced increases in plasma levels of catecholamines.

Adult↗
PubMed1991

Effects of succinylcholine on the pharmacodynamics of pipecuronium and pancuronium.

To study the effects of succinylcholine on subsequent pharmacodynamics of nondepolarizing muscle relaxants, a comparative pharmacodynamic study was carried out in patients having balanced anesthesia (thiopental, fentanyl, nitrous oxide/oxygen) in whom equipotent doses of pipecuronium (80 micrograms/kg) and pancuronium (100 micrograms/kg) were given with or without prior administration of succinylcholine (1 mg/kg). Fifty-two patients were randomly assigned to one of the following four groups: 1, pancuronium (100 micrograms/kg); 2, pipecuronium (80 micrograms/kg); 3, succinylcholine (1 mg/kg) plus pancuronium (100 micrograms/kg); and 4, succinylcholine (1 mg/kg) plus pipecuronium (80 micrograms/kg). In groups 3 and 4, the nondepolarizing relaxant was given after succinylcholine when the twitch height recovered to 75% of its control value. For maintenance of neuromuscular blockade, additional increments of pancuronium (20 micrograms/kg) or pipecuronium (15 micrograms/kg) were given. Neuromuscular function was monitored throughout induction, maintenance, spontaneous recovery, and pharmacologic reversal of the neuromuscular block. Mean onset times for pancuronium (group 1) and pipecuronium (group 2) given without succinylcholine were (mean +/- SEM) 2.5 +/- 0.3 and 2.8 +/- 0.2 min, respectively. Mean onset times (times to maximum twitch depression) of the two drugs given after succinylcholine (groups 3 and 4) were significantly shorter (1.4 +/- 0.4 and 1.6 +/- 0.1 min, respectively). Clinical durations (i.e., until 25% twitch recovery of pancuronium and pipecuronium) were not significantly different among the four groups, varying from 81.1 +/- 5.4 (group 4) to 107.0 +/- 17.0 (group 2) min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗