Cisatracurium

Class	Non-depolarising NMJ blocker
Chemistry	Benzylisoquinolinium diester
Routes of administration	IV only
Absorption	Poor absorption; minimal oral bioavailability
Solubility	pKa=19.02; good water solubility
Distribution	VOD= 0.20 L/kg, 38% protein bound
Metabolism	Metabolised by plasma esterase and spontaneously degraded by temperature-sensitive Hofmann degradation
Elimination	Minimal renal or hepattic clearance
Time course of action	Half life 26 minutes
Target receptor	Nicotinic acetylcholine receptors at the neuromuscular junction
Mechanism of action	Nondepolarising neuromuscular junction blocker (competitive antagonist of acetylcholine); by binding to the nicotinic acetylcholine receptor, this agent blocks the binding of acetylcholine, and prevents the cation channel from opening, thus preventing the depolarisation of the motor endplate.
Clinical effects	Nondepolarising neuromuscular junction blockade; No autonomic effects (i.e no ganglionic blockade or vagolytic effects) However, des cause hypotension via systemic histamine release. Also, breakdown product (laudanosine) lowers the seizure threshold - but because of higher potency, about five times less laudanosine is produced from cisatracurium, as compared to atracurium
Literature reference	Bryson et al (1997)
CICM details of understanding	Level 1
Mentioned around Deranged Physiology	Pharmacology of neuromuscular blocking drugs
Related SAQs	Question 13 from the second paper of 2018 (roc vs cis)