Musculoskeletal Agents
Skeletal Muscle Relaxants
Neuromuscular blockers

Description: Rocuronium is a short-acting, nondepolarizing, neuromuscular blocking drug. It was developed out of a need for an agent with a rapid onset and short duration of action, and a low risk of side effects. Rocuronium's onset of action is comparable to that of succinylcholine, but its duration of action is significantly longer. Due to its rapid onset, rocuronium may be a useful alternative to succinylcholine for rapid sequence induction in certain situations. Compared with other nondepolarizing agents, rocuronium has a more rapid onset of action. Rocuronium also produces minimal histamine release. Rocuronium was approved by the FDA in March 1994.

Mechanism of Action: Nondepolarizing agents such as rocuronium produce skeletal muscle paralysis by competing with acetylcholine for cholinergic receptor sites at the myoneural junction. Unlike depolarizing agents, rocuronium has little agonist activity at the motor endplate. Skeletal muscle relaxation proceeds in predictable order, starting with muscles associated with fine movements, e.g., eyes, face, and neck. These are followed by muscles of the limbs, chest, and abdomen and, finally, the diaphragm. Larger doses increase the risk of developing respiratory depression due to relaxation of the intercostal muscles and diaphragm. Muscle tone returns in the reverse order.

In addition to its therapeutic actions, rocuronium can cause an increase in heart rate, but this is minimal at normal doses. Rocuronium produces little histamine release and no ganglion blockade, so hypotension and bronchospasm are not associated with its use. Children generally require larger mg/kg doses than adults to achieve muscle relaxation. The muscle weight-to-body weight ratio, the volume of extracellular fluid, and renal function also contribute to response.

Pharmacokinetics: Rocuronium is administered intravenously. Following administration, rocuronium is distributed into the extracellular space. It is not distributed into fat reserves. The half-life is 1—2 minutes during the rapid distribution phase and 14—18 minutes during the slower distribution phase. This second distribution phase accounts for the need to reduce the maintenance rate to almost 20% of the initial infusion rate. Duration of clinical effect is similar in patients with normal or impaired renal function. In patients with hepatic impairment, however, the clinical duration can be up to 1.5 times that of patients with normal hepatic function due to increased volume of distribution in patients with hepatic impairment. Protein binding of rocuronium is about 30%.

Metabolism of rocuronium occurs in the liver. The plasma half-life of rocuronium in patients with normal renal and hepatic function is about 2.4 hours during isoflurane anesthesia. The plasma half-life in patients with hepatic cirrhosis is 4.3 hours during isoflurane anesthesia. In pediatric patients ranging from age 4 months to 8 years, rocuronium's plasma half-life averaged about 1.1 hours during halothane anesthesia.

Physical Structure

This monoquaternary steroid analogue of vecuronium was designed to provide a rapid onset of action.

Metabolism & Excretion

Rocuronium undergoes no metabolism and is eliminated primarily by the liver and slightly by the kidneys. Its duration of action is not significantly affected by renal disease, but it is modestly prolonged by severe hepatic failure and pregnancy. Because rocuronium does not have active metabolites, it may be a better choice than vecuronium for prolonged infusions (eg, the intensive care unit setting). Elderly patients may experience a prolonged duration of action due to decreased liver mass.


Rocuronium is less potent than most other steroidal muscle relaxants (potency appears to be inversely related to speed of onset). It requires 0.45–0.9 mg/kg intravenously for intubation and 0.15 mg/kg boluses for maintenance. A lower dose of 0.4 mg/kg may allow reversal as soon as 25 min after intubation. Intramuscular rocuronium (1 mg/kg for infants; 2 mg/kg for children) provides adequate vocal cord and diaphragmatic paralysis for intubation, but not until after 3–6 min (deltoid injection has a faster onset than quadriceps), and can be reversed after about 1 h. Rocuronium can produce a prolonged duration of action in elderly patients. Initial dosage requirements are modestly increased in patients with advanced liver disease, presumably due to a larger volume of distribution.

Side Effects & Clinical Considerations

Rocuronium (at a dose of 0.9–1.2 mg/kg) has an onset of action that approaches succinylcholine (60–90 s), making it a suitable alternative for rapid-sequence inductions, but at the cost of a much longer duration of action. This intermediate duration of action is comparable to vecuronium or atracurium.

Some clinicians compensate for rocuronium's longer onset of action (compared with that of succinylcholine) by administering it 20 s before propofol or thiopental (the "timing principle"). Disadvantages to this technique include the possibility of delayed administration of induction agent (eg, due to intravenous line precipitate) resulting in a conscious but paralyzed patient.

Rocuronium (0.1 mg/kg) has been shown to be a rapid (90 s) and effective agent (decreased fasciculations and postoperative myalgias) for precurarization prior to administration of succinylcholine. It has slight vagolytic tendencies.

Rocuronium is an aminosteroid neuromuscular relaxant. It has one sixth the potency of vecuronium, a more rapid onset, but a similar duration of action and similar pharmacokinetic behavior. Bartkowski et al showed that, with equipotent doses, rocuronium onset at the adductor pollicis was much faster than that of atracurium and vecuronium. After doses of 600 mcg•kg-1 (2 x ED95, 4 x ED50) maximal block occurs in ~60–90 s and Pühringer et al were unable to detect any difference in tracheal intubating conditions 60 s after succinylcholine, 1 mg•kg-1, or rocuronium, 0.6 mg•kg-1, during balanced anesthesia. As for other nondepolarizing relaxants the onset of action of rocuronium is more rapid at the diaphragm than at the adductor pollicis, and approximately twice as much is required to produce the same degree of paralysis. The potency, onset time, recovery index, and duration of action are similar in infants, children, and adults during nitrous oxide–alfentanil anesthesia in contrast to vecuronium, which is a long-acting relaxant in infants.

CARDIOVASCULAR EFFECTS. No hemodynamic changes (blood pressure, heart rate, or ECG) were seen in humans, and there were no increases in plasma histamine concentrations after doses of up to 4 times ED95. Similarly, when rocuronium 0.6 mg•kg-1 was given to patients before coronary artery bypass grafting the slight hemodynamic changes observed were no different from those following equivalent doses of vecuronium.
CLINICAL USE. The rapid onset and intermediate duration of action makes this agent a potential replacement for succinylcholine in conditions where rapid tracheal intubation is indicated. Also, it is likely that rocuronium will replace vecuronium where an intermediate-duration relaxant without cardiovascular effects is required. Initial doses of 0.6 mg•kg-1 iv will usually produce good intubating conditions within 90 s. Subsequent doses of 0.075–0.225 mg•kg-1 will provide clinical relaxation for 10–20 min, respectively. Alternatively, rocuronium might be given by continued infusion, titrated with the help of a nerve stimulator.