The Role of the Non-Depolarizing Drugs in the Prevention of Suxamethonium Bradycardia

Abstract

Evidence has been presented to show that a second dose of suxamethonium is capable of producing a severe bradycardia in man. This response may be effectively prevented by the prior administration of certain non-depolarizing muscle relaxants namely tubocurarine, alcuronium, c-toxiferine and pancuronium in quantities of one-quarter or less of their muscle relaxant level. It is suggested that suxamethonium causes altered cardiac rhythm by stimulation of afferent vagal receptors, which action may be blocked by tubocurarine and similar drugs.

Pediatric Rapid Sequence Intubation

“…[6][7][8]14 Atropine appears to be effective in preventing the bradycardia associated with the administration of succinylcholine [6][7][8]14 Atropine appears to be effective in preventing the bradycardia associated with the administration of succinylcholine …”

The Effect of Succinylcholine on the Isolated Mammalian Heart

“…Bradycardia most frequently occurs with the second or subsequent dose of succinylcholine. This has been reported as frequently as 80% in one series of cases (Mathias et al 1970). Succinylcholine may cause profound negative chronotropy after the administration of a single injection in certain 'at risk' groups of patientsthe badly burned subject (Tolmie et al 1967, Belin & Karleen 1966, small children (Leigh et al 1957), digitalized patients (Dowdy & Fabian 1963) and following damage to the spinal cord (Smith & Grenvik 1970).…”

“…In man the most commonly reported action of succinylcholine on the cardiovascular system is a negative chronotropic one (Beretervide 1955, Johnstone 1955, Leigh et al 1957, Lupprian & Churchill-Davidson 1960, Williams et al 1961, Galindo & Davis 1962, Gologorsky & Umanov 1970, Mathias et al 1970. Less frequently reported are hypotension (Adams & Hall 1962, Williams et al 1961, hypertension (Galindo & Davis 1962) and ventricular extrasystoles and ventricular fibrillation (Tolmie et al 1967, Belin & Karleen 1966, Vanner et al 1970, Dowdy & Fabian 1963.…”

“…These differ as to the precise action of the drug, and there are also numerous diverse theories about its site of action. Complications have occurred with the clinical use of succinylcholine, including bradycardia (Johnstone 1955, Beretervide 1955, Leigh et al 1957, Williams et al 1961, Galindo & Davis 1962, Tolmie et al 1967, Gologorsky & Umanov 1970, Mathias et al 1970, tachycardia (Beretervide 1955, Lupprian & Churchill-Davidson 1960, Conway 1961, Adams & Hall 1962, Galindo & Davis 1962, hypotension (Paton 1959, Adams & Hall 1962, Galindo & Davis 1962 and hypertension (Beretervide 1955, Johnstone 1955, Paton 1959, Conway 1961, Williams et al 1961, Galindo & Davis 1962, Goodman & Gilman 1965. More serious cardiac effects have also been reported, including ventricular arrhythmias (Lupprian & Churchill-Davidson 1960, Dowdy & Fabian 1963, Vanner et al 1970) and ventricular fibrillation and arrest (Tolmie et al 1967, Belin & Karleen 1966, Vanner et al 1970.…”

“…It has been suggested that the bradycardia following succinylcholine administration is a reflex action secondary to stimulation of the 10 Section ofAnesthetics pressor receptors in the carotid sinus by the drug in an atypical respon; (Mathias et al 1970). This would explain the con-produced by succinylch flicting reports of changes in arterial pressure the level of K+ in t] following succinylcholine administration in man, possibly the further: since no change in blood pressure would be resulting from depo required to effect this baroreceptor reflex.…”