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At least 19 recordsLinked to original sources
PubMed1982

Cardiac effects of self-taming of succinylcholine and repeated succinylcholine administration.

Pretreatment with small (10 mg) doses of succinylcholine ("self-taming") decreases the incidence of muscle fasciculations following succinylcholine administration and may decrease the incidence of other unwanted effects. This study was designed to assess the cardiac effects of such self-taming and to assess the degree of protection afforded against bradydysrhythmias following subsequent succinylcholine administration. Sixty patients were studied and allocated randomly to three groups of twenty. Each group was assigned a different form of pretreatment. Patients in group I received 10 mg of succinylcholine immediately after induction. Patients in group II were treated with d-tubocurarine 0.04k mg . kg-1 three minutes before induction. Patients in group III received no pretreatment. All patients were induced with thiopentone 4 mg . kg-1 followed by succinylcholine 1 mg . kg-1 45 seconds later. A second dose of succinylcholine 1 mg . kg-1 was administered to the patients in the two pretreatment groups between four and five minutes after the first dose of succinylcholine. Following both the first and second doses of succinylcholine patients in the self-taming group showed a significantly greater incidence of bradydysrhythmias when compared to the other two groups. It is concluded that the use of a self-taming technique is potentially hazardous, and that it does not confer protection against repeated succinylcholine administration.

Anesthesia↗
PubMed1994

Probable succinylcholine-induced hyperkalemia in a trauma victim after recent benign anesthetics with succinylcholine.

Throughout its pharmacological history in anesthesia practice, succinylcholine has been notorious for its role in causing life-threatening hyperkalemia. Normally the serum potassium level will increase .5 to 1.0 mEq/L because of a sustained opening of the receptors in the neuromuscular junction and release of myoplasmic potassium. However, in certain patients the drug will result in a much higher level of serum potassium. The literature points out numerous conditions that predispose particular patients to this exaggerated intensification of potassium leakage from within the cell. Traumatized, neuromuscular diseased, infected, exsanguinated, acidotic, and closed head injury patients among this list. This case report describes a trauma patient requiring numerous orthopedic repairs in a relatively short period of time. He received succinylcholine on three separate occasions within a 20-day span without any untoward effects. However, during his sixth surgery and the fourth administration of succinylcholine, he developed ventricular fibrillation requiring defibrillation and cardiopulmonary resuscitation before converting to a sinus tachycardia. After ruling out other causes of the arrhythmia, the most probable one was hyperkalemia. A possible explanation of this probable succinylcholine-induced hyperkalemia may have been a combination of the trauma, tissue wasting, infection, immobility, or acute respiratory acidosis. The potassium elevation was treated successfully with hyperventilation, calcium chloride, sodium bicarbonate, glucose, and insulin. The patient recovered without complications and was later discharged to home. Succinylcholine definitely has its use in anesthesia, but it is imperative for the provider to be discriminatory in its administration. An all-encompassing history is paramount to discover any hidden rationale not to use succinylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Comparative study of induction with propanidid plus succinylcholine and thiopental plus succinylcholine].

A comparative study was carried out in a group of patients on induction obtained by Propanidid + succinylcholine and by Thiopental + succinylcholine. Serum potassium variations were determined before narcosis and 2 and 4 minutes after succinylcholine. The study was done by means of Student's parameter noting unsignificant and significant increases and decreases, comparing the treated lots with the control lot, and the lots in terms of time, therefore the dynamic evolution of the process and the lots in terms of the drugs. It is demonstrated that in the patients with a high potassium intracellular release potential, the Propanidid + succinylcholine combination is more advantageous.

Adult↗
PubMed2001

Cost identification analysis for succinylcholine.

UNLABELLED: The cost of a dose of succinylcholine from society's perspective equals the acquisition cost of the drug plus the cost of its adverse outcomes. We hypothesized that although the acquisition cost of succinylcholine is minimal, the true cost would be much larger. We reviewed the medical literature to identify the total cost of a dose of succinylcholine when administered for nonemergency purposes according to manufacturers' guidelines (i.e., to adults only). We found that 88% of the cost per dose of succinylcholine was for the chance of dying or sustaining permanent brain injury from anaphylactic or anaphylactoid reactions to succinylcholine. Consequently, the estimated cost per dose of succinylcholine was sensitive to the incidence of anaphylactic or anaphylactoid reactions to succinylcholine, the risk of severe injury from anaphylactic or anaphylactoid reactions, and the financial value of unforeseen instant death or permanent brain injury. The range for the cost per dose of succinylcholine was thus large, $9 to $93. Our best estimate of the cost per dose was $37. We conclude that the true cost per dose of succinylcholine from society's perspective is more than 20 times the acquisition cost. However, a precise costing requires better knowledge of the incidence and consequences of anaphylactic or anaphylactoid reactions to succinylcholine. IMPLICATIONS: The true cost of succinylcholine is more than 20 times the acquisition cost of the drug. The estimated cost is very sensitive to the risk and cost of patients dying or sustaining brain injury from anaphylactic or anaphylactoid reactions to succinylcholine.

Anaphylaxis↗
PubMed2003

Optimal dose of succinylcholine revisited.

BACKGROUND: The authors reappraised the conventional wisdom that the intubating dose of succinylcholine must be 1.0 mg/kg and attempted to define the lower range of succinylcholine doses that provide acceptable intubation conditions in 95% of patients within 60 s. METHODS: This prospective, randomized, double-blind study involved 200 patients. Anesthesia was induced with 2 mug/kg fentanyl and 2 mg/kg propofol. After loss of consciousness, patients were randomly allocated to receive 0.3, 0.5, or 1.0 mg/kg succinylcholine or saline (control group). Tracheal intubation was performed 60 s later. A blinded investigator performed all laryngoscopies and also graded intubating conditions. RESULTS: Intubating conditions were acceptable (excellent plus good grade combined) in 30%, 92%, 94%, and 98% of patients after 0.0, 0.3, 0.5, and 1.0 mg/kg succinylcholine, respectively. The incidence of acceptable intubating conditions was significantly greater (P < 0.05) in patients receiving succinylcholine compared with those in the control group but was not different among the different succinylcholine dose groups. The calculated doses of succinylcholine (and their 95% confidence intervals) that were required to achieve acceptable intubating conditions in 90% and 95% of patients at 60 s were 0.24 (0.19-0.31) mg/kg and 0.56 (0.43-0.73) mg/kg, respectively. CONCLUSIONS: The use of 1.0 mg/kg of succinylcholine may be excessive if the goal is to achieve acceptable intubating conditions within 60 s. Comparable intubating conditions were achieved after 0.3, 0.5, or 1.0 mg/kg succinylcholine. In a rapid-sequence induction, 95% of patients with normal airway anatomy anesthetized with 2 mug/kg fentanyl and 2 mg/kg propofol should have acceptable intubating conditions at 60 s after 0.56 mg/kg succinylcholine. Reducing the dose of succinylcholine should allow a more rapid return of spontaneous respiration and airway reflexes.

Adult↗
PubMed2006

Activation and inhibition of human muscular and neuronal nicotinic acetylcholine receptors by succinylcholine.

BACKGROUND: Succinylcholine is one of the most widely used muscle relaxants in clinical anesthesia and emergency medicine. Although the clinical advantages and cardiovascular side effects are well known, its mechanism of action within the human nicotinic cholinergic receptor system remains to be understood. The aim of this study was to investigate the effect of succinylcholine on human muscle and neuronal nicotinic acetylcholine receptor (nAChR) subtypes. METHODS: Xenopus laevis oocytes were injected with human messenger RNA for muscle and neuronal nAChR subunits. Receptor activation, desensitization, and inhibition induced by the natural ligand acetylcholine or by succinylcholine was studied using a multichannel two-electrode voltage clamp setup. Responses were measured as peak current and net charge. RESULTS: Succinylcholine concentration-dependently activated the muscle-type nAChR with an EC50 value of 10.8 microm (95% confidence interval, 9.8-11.9 microm), and after the initial activation, succinylcholine desensitized the muscle-type nAChR. Succinylcholine did not activate the neuronal nAChR subtypes alpha3beta2, alpha3beta4, alpha4beta2, or alpha7 at concentrations up to 1 mm and was a poor inhibitor at these receptor subtypes, with IC50 values above 100 microm. CONCLUSION: Succinylcholine activates the muscle-type nAChR followed by desensitization. The observation that succinylcholine does not inhibit the presynaptic alpha3beta2 autoreceptor at clinically relevant concentrations provides a possible mechanistic explanation for the typical lack of tetanic fade in succinylcholine-induced neuromuscular blockade. Finally, cardiovascular side effects (e.g., tachyarrhythmias) of succinylcholine are not mediated via direct activation of the autonomic ganglionic alpha3beta4 subtype because succinylcholine does not activate the neuronal nAChRs.

Acetylcholine↗
PubMed2000

Malignant hyperthermia phenotype: hypotension induced by succinylcholine in susceptible swine.

BACKGROUND: Succinylcholine causes immediate and severe arterial hypotension in swine with the malignant hyperthermia phenotype. The underlying mechanisms are unknown. METHODS: Malignant hyperthermia-susceptible (MHS; n = 10) and normal swine (n = 5) were anesthetized with thiopental. The following were monitored: electrocardiogram; arterial blood pressure; pulmonary artery, central venous, and left and right ventricular pressure; cardiac output; end-tidal carbon dioxide; core temperature; peripheral-blood flows; and arterial blood gases. After a control period, 2 mg/kg succinylcholine was given intravenously. Three MHS animals received 1 mg/kg vecuronium and two MHS animals received 2.5 mg/kg dantrolene intravenously. The effects of succinylcholine on left and right ventricular pressure and contractility were analyzed in isolated hearts. The effects of 0.06 mm succinylcholine on isometric tension development were recorded in isolated femoral artery rings. RESULTS: Succinylcholine caused an early, severe decrease in blood pressure, cardiac output, left ventricular pressure, and left ventricular contractility in MHS swine but not in normal swine; no significant differences were found in heart rate, right ventricular parameters, systemic vascular resistance, and preload (pulmonary diastolic pressure, central venous pressure). The succinylcholine-induced hypotension and associated effects were not prevented by dantrolene. However, pretreatment with high-dose vecuronium prevented not only the cardiovascular depression, but also MH. In addition, no phenotypic differences of succinylcholine on contractility or left ventricular pressure were observed in the isolated working hearts. Similary, succinylcholine did not cause a significantly different relaxation in rings in either phenotype. CONCLUSION: Succinylcholine-induced hypotension occurred before muscle hypermetabolism in MHS swine. Succinylcholine had no differential physiologic effects on either the isolated heart or on isolated arteries. This hypotension could not be prevented by dantrolene but was prevented by pretreatment with high-dose vecuronium. Thus, an indirect mechanism such as the release of a cardiac depressant from skeletal muscle may have caused this hypotensive response.

Animals↗
PubMed1989

Comparison of tracheal intubating conditions and neuromuscular blocking profiles after intubating doses of mivacurium chloride or succinylcholine in surgical outpatients.

Thirty ASA physical status I or II outpatients scheduled to undergo short procedures (less than 1 hr in duration) requiring tracheal intubation received either 1.0 mg/kg succinylcholine or 0.20 mg/kg (2.5 x ED95) or 0.25 mg/kg (3 x ED95) mivacurium. A N2O/O2/narcotic anesthetic technique was utilized and the ulnar nerve was stimulated with subcutaneous electrodes placed at the wrist. Tracheal intubation was attempted in all patients either 2 min after mivacurium or 1 min after succinylcholine. Intubation conditions were not different between the succinylcholine and mivacurium groups or between the two mivacurium groups. The onset and duration of neuromuscular blockade were shorter with succinylcholine than with mivacurium. Suppression of the T1 response to 90% of baseline occurred in 0.9 min with 1.0 mg/kg succinylcholine and at 2.2 and 1.5 min respectively, with 0.20 mg/kg and 0.25 mg/kg mivacurium. Initial recovery of the T1 response occurred at 6.4 min after 1.0 mg/kg succinylcholine and 12.7 and 13.6 min respectively after 0.20 mg/kg and 0.25 mg/kg mivacurium. Subsequent to initial recovery from the intubating dose of relaxant, infusions of mivacurium or succinylcholine were administered to maintain approximately 95% block. The mean infusion rates were 6.6 micrograms.kg-1.min-1 mivacurium and 41.2 micrograms.kg-1.min-1 for succinylcholine. Spontaneous recovery from neuromuscular blockade occurred more quickly after succinylcholine than after mivacurium: the time from cessation of infusion to recovery of T1 to 95% of baseline was 6.5 min in patients given succinylcholine and 16.7 min in patients given mivacurium. When reversal was in order, residual mivacurium-induced blockade was readily antagonized by 0.045 mg/kg neostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Rocuronium versus succinylcholine for rapid sequence induction intubation.

BACKGROUND: Patients requiring emergent endotracheal intubation often require a rapid sequence induction intubation (RSI) technique to protect against gastric aspiration, to facilitate intubation, or to protect against increased intracranial pressure. Succinylcholine is the most common muscle relaxant used because it has a fast onset and a short duration. Unfortunately it can have serious side effects as a result of it's membrane depolarizing effect and release of potassium. Rocuronium has been suggested to create intubating conditions similar to succinylcholine. Previous studies have been underpowered to determine equivalence and there has been no previous meta-analysis performed. OBJECTIVES: To determine if rocuronium creates comparable intubating conditions to succinylcholine during RSI intubation. Comparisons were made with succinylcholine based on the dose of rocuronium, use of a narcotic, emergent versus elective intubation, age group and the induction agent used. The primary outcome was excellent intubation conditions. A secondary outcome of clinically acceptable conditions was also performed. These were all dichotomous outcomes using cutpoints from a four point scale by Goldberg to evaluate intubation conditions. SEARCH STRATEGY: We searched MEDLINE (1966-March 2000), EMBASE (1988-March 2000) and the Cochrane Central Register of Controlled Trials (CENRAL) (March 2000) for randomized controlled trials (RCT) or controlled clinical trials (CCT) relating to the use of rocuronium and succinylcholine. Foreign language journals were included. References of identified studies were hand-searched for citations missed by the electronic searches. SELECTION CRITERIA: All trials meeting the inclusion criteria (comparison of rocuronium and succinylcholine, one of study's main outcomes was scoring of intubation conditions) were included. DATA COLLECTION AND ANALYSIS: Data were extracted and methodological quality was assessed independently by two reviewers for allocation concealment. The outcomes were combined using MetaView 4.1 with risk differences for all categories and RR for the excellent outcomes with a random effects model. MAIN RESULTS: 40 studies were identified; 26 were combined for analysis. Overall, rocuronium was inferior to succinylcholine, with a RR=0.87 (95%CI = 0.81 to 0.94) (N=1606). In the group that used propofol for induction of anaesthesia, the intubation conditions were similar, with a RR=0.96 (95%CI = 0.87 to 1.06) (N=640). No major adverse events were reported. REVIEWER'S CONCLUSIONS: Succinylcholine created superior intubation conditions to rocuronium when comparing excellent intubation conditions. Using the less stringent outcome, clinically acceptable intubation conditions, the two agents were not statistically different. Intubation conditions were not statistically different between succinylcholine and rocuronium when propofol was used.

Androstanols↗