| Indication |
For inpatients and outpatients as an adjunct to general anesthesia
to facilitate both rapid sequence and routine tracheal intubation, and
to provide skeletal muscle relaxation during surgery or mechanical
ventilation. |
| Pharmacodynamics |
Neuromuscular blocking agents are drugs that cause skeletal
muscle relaxation primarily by causing a decreased response to the
neurotransmitter acetylcholine (ACh) at the myoneural (neuromuscular)
junction of skeletal muscle. At that site, ACh normally produces
electrical depolarization of the postjunctional membrane of motor
end-plate, which leads to conduction of muscle action potential and
subsequently induces skeletal muscle contraction. Neuromuscular agents
are classified as depolarizing or nondepolarizing. Rocuronium is a
nondepolarizing neuromuscular blocking agent with a rapid to
intermediate onset depending on dose and intermediate duration.
Rocuronium, like vecuronium is longer acting in infants than in
children. However, unlike vecuronium, rocuronium retains the
characteristics of an intermediate-acting NMBD in infants. |
| Mechanism of action |
Rocuronium acts by competing for cholinergic receptors at the
motor end-plate. This action is antagonized by acetylcholinesterase
inhibitors, such as neostigmine and edrophonium. Rocuronium acts by
competitively binding to nicotinic cholinergic receptors. The binding of
vecuronium decreases the opportunity for acetylcholine to bind to the
nicotinic receptor at the postjunctional membrane of the myoneural
junction. As a result, depolarization is prevented, calcium ions are not
released and muscle contraction does not occur. Evidence also suggests
that nondepolarizing agents can affect ACh release. It has been
hypothesized that nondepolarzing agents bind to postjunctional
("curare") receptors and may therefore interfere with the sodium and
potassium flux, which is responsible for depolarization and
repolarization of the membranes involved in muscle contraction. |
| Absorption |
Poorly absorbed from the GI tract. |
| Volume of distribution |
- 0.3 L/kg [3 to <12 mos]
- 0.26 L/kg [1 to <3 yrs]
- 0.21 L/kg [3 to <8 yrs]
|
| Protein binding |
Approximately 30% bound to human plasma proteins. |
| Metabolism |
Rocuronium is metabolized to a less active metabolite, 17-desacetyl-rocuronium, and is eliminated primarily by the liver. |
| Route of elimination |
Studies of distribution, metabolism, and excretion in cats and
dogs indicate that rocuronium is eliminated primarily by the liver. |
| Half life |
The rapid distribution half-life is 1-2 minutes and the slower
distribution half-life is 14-18 minutes. Renal impairment has no net
effect on half-life, however, half-life is almost doubled in patients
with impaired liver function. |
| Clearance |
- 0.25 L/kg/hr [Adults (Ages 27 to 58 years)]
- 0.21 L/kg/hr [Geriatrics (>=65 yrs)]
- 0.16 L/kg/hr [Normal ewnal and hepatice function]
- 0.13 L/kg/hr [Renal transplant patients]
- 0.13 L/kg/hr [Hepatic dysfunction patients]
- 0.35 +/- 0.08 L/kg/hr [Pediatric Patients 3 to <12 mos]
- 0.32 +/- 0.07 L/kg/hr [Pediatric Patients 1 to 3 yrs]
- 0.44 +/- 0.16 L/kg/hr [Pediatric Patients 3 to 8 yrs]
|
| Toxicity |
No cases of significant accidental or intentional overdose have
been reported. Overdosage with neuromuscular blocking agents may result
in neuromuscular block beyond the time needed for surgery and
anesthesia. |
