Compare and contrast rocuronium and cisatracurium
This question was best answered using a tabular format outlining class of drug, pharmaceutics, pharmacokinetics, reversibility and side effects. Better answers commented on the significance of the differences between the two agents and its relevance to ICU practice. Many candidates confused these muscle relaxants with each other and with depolarising muscle relaxants
|Class||Non-depolarising NMJ blocker||Non-depolarising NMJ blocker|
|Routes of administration||IV or IM only||IV only|
|Absorption||Poor absorption; minimal oral bioavailability||Poor absorption; minimal oral bioavailability|
|Solubility||pKa=7.96; good water solubility||pKa=19.02; good water solubility|
|Distribution||VOD=0.27L, 46% protein-bound||VOD= 0.20 L/kg, 38% protein bound|
|Target receptor||Nicotinic acetylcholine receptors at the neuromuscular junction||Nicotinic acetylcholine receptors at the neuromuscular junction|
|Metabolism||Minimal metabolism (less than 1%)||Metabolised by plasma esterase and spontaneously degraded by temperature-sensitive Hofmann degradation|
|Elimination||Around 90% is cleared by being excreted into bile, and the rest is cleared renally||Minimal renal or hepatic clearance|
|Time course of action||Half-life 60-100 minutes||Half life 26 minutes|
|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.||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; also:
- Basically no ganglionic effects
- Minimal vagolytic effect (slight increase in HR)
- Minimal sympathomimetic effect (slight increase in HR)
- No histamine release
- Some risk of anaphylaxis (incidence is 1:3,500 to 1:445,000).
|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
|Single best reference for further information||Wicks (1994)||Bryson et al (1997)|
|Utility in the ICU||Rapid onset of effect makes this ideal for rapid sequence induction, but tendency to accumulate in hepatic and renal failure makes it a poor choice for prolonged infusions||Organ-independent clearance makes this agent ideal for prolonged sustained infusions, but the slow onset of effect makes it a poor choice for rapid sequence induction|
Wicks, TERRY C. "The pharmacology of rocuronium bromide (ORG 9426)." AANA journal 62.1 (1994): 33-38.
Bryson, Harriet M., and Diana Faulds. "Cisatracurium besilate: a review of its pharmacology and clinical potential in anaesthetic practice." Drugs 53 (1997): 848-866.
Lee, C. "Structure, conformation, and action of neuromuscular blocking drugs." British Journal of Anaesthesia 87.5 (2001): 755-769.