Pharmacology: Competitive neuromuscular blockers act by competing with acetylcholine for receptors on the motor end plate of the neuromuscular junction to produce blockade. The muscles that produce fine rapid movements such as those of the face are the first to be affected followed by those of the limbs and torso; the last to be affected are those of the diaphragm. The paralysis is reversible with recovery occurring in reverse order. Restoration of normal neuromuscular function can be hastened by increasing the concentration of acetylcholine at the motor end plate by giving an anticholinesterase such as neostigmine.
Pharmacodynamics: Atracurium is a highly selective competitive (non-depolarizing) neuromuscular blocking agent with an intermediate duration of action.
Non-depolarizing agents antagonize the neurotransmitter action of acetylcholine by binding with receptor sites on the motor-end plate.
Atracurium can be used in a wide range of surgical procedures and to facilitate controlled ventilation.
Pediatric population: The limited data in neonates from literature reports suggest variability in the time to onset and duration of action of Atracurium in this population as compared to children.
Pharmacokinetics: Following intravenous injection, Atracurium undergo spontaneous degradation via Hofman elimination (a non-enzymatic breakdown process occurring at physiological pH and temperature) to produce laudanoside and other metabolites. There is also hydrolysis by non-specific plasma esterases. The metabolites have no neuromuscular blocking activity.
About 80% of atracurium is bound to plasma proteins. Atracurium and its metabolites cross the placenta in clinically insignificant amounts.
Excretion of Atracurium is in urine and bile, mostly as metabolites. The elimination half-life has been reported to be approximately 20 minutes for atracurium.