Vecuronium Bromide

Specific Drugs

Absorption

Bioavailability

Poorly absorbed from the GI tract.b

Onset

Time to maximum neuromuscular blockade decreases as the dose increases.1 2 17 18 26 46 69 70 87

Following IV administration of 0.08–0.1 mg/kg, neuromuscular blockade begins within 1 minute and is maximal at 3–5 minutes.1 2

Duration

Duration of neuromuscular blockade increases as the dose increases.1 2 17 47 70 80 87

Duration of clinically sufficient neuromuscular blockade induced by initial dose of 0.08–0.1 mg/kg under balanced or halothane anesthesia is about 25–30 or 30–40 minutes, respectively.2

Spontaneous recovery to about 25% of baseline generally occurs within 25–40 minutes under balanced anesthesia and is usually 95% complete 45–65 minutes after administration.1

The time necessary for 25–75% recovery from neuromuscular blockade following doses of 0.08–0.1 mg/kg under balanced or halothane anesthesia is about 15–25 minutes;1 144 recovery time following initial doses appears to be dose dependent.17 141

Special Populations

Hepatic dysfunction (i.e., cirrhosis, cholestasis) may prolong duration of and rate of recovery from neuromuscular blockade.1 38 79 90

In patients with severe renal impairment who have not undergone dialysis prior to surgery, duration of neuromuscular blockade may be prolonged.1 2

In geriatric patients, increased time of onset31 and decreased rate of recovery from neuromuscular blockade.30 32 33

In patients undergoing cardiopulmonary bypass surgery under induced hypothermia, duration of neuromuscular blockade may be prolonged.152

Distribution

Extent

Appears to rapidly distribute into extracellular space.2 100 Undergoes rapid and extensive hepatic extraction.116 Crosses the placenta minimally;94 95 96 97 not known whether distributed into milk.144

Plasma Protein Binding

Approximately 60–90%.1 2 57 99

Special Populations

In children <1 year of age, volume of distribution is increased.148 In geriatric patients, volume of distribution may be decreased.100 In patients with renal failure, volume of distribution may be slightly increased.74 84 104

Elimination

Metabolism

Metabolic fate not fully characterized in humans.1 2 3 106 116 143 In vitro, vecuronium undergoes spontaneous deacetylation to form hydroxy derivatives.9

Elimination Route

Excreted principally in feces via biliary elimination;1 38 79 90 143 also excreted in urine.1 2 106 116

Half-life

Biphasic;1 3 18 26 38 84 94 95 98 104 terminal elimination half-life averages 65–75 minutes.1

Special Populations

In patients with cirrhosis, half-life averages 84 minutes.38

In patients with renal failure, half-life not substantially altered;84 104 potential for high plasma concentrations of 3-desacetyl vecuronium (neuromuscular blocking activity is ≥50% of that of vecuronium).186 187 189 190 84 104

During late pregnancy, half-life decreases to about 35–40 minutes.1 2 94 95

Storage

Parenteral

15–30°C; protect from light.1 2

Following reconstitution with bacteriostatic water for injection containing benzyl alcohol, 2–8°C or room temperature (<30°C) for 5 days.1

Following reconstitution with sterile water for injection or other compatible solution (see Solution Compatibility under Stability), 2–8°C for 24 hours.1

Compatibility

For information on systemic interactions resulting from concomitant use, see Interactions.

Parenteral

Unstable in the presence of bases.10 11

• Produces skeletal muscle relaxation by causing a decreased response to acetylcholine (ACh) at the myoneural (neuromuscular) junction of skeletal muscle.b

• Exhibits high affinity for ACh receptor sites and competitively blocks access of ACh to motor end-plate of myoneural junction; may affect ACh release.b

• Blocks the effects of both the small quantities of ACh that maintain muscle tone and the large quantities of ACh that produce voluntary skeletal muscle contraction; does not alter the resting electrical potential of the motor end-plate or cause muscular contractions.b

• Exhibits minimal cardiovascular effects.1 3 5 6 19 145

• Appears to have little histamine-releasing activity.1 4 12 18 19 48 49 50 52 143 147 A less potent stimulator of histamine release than atracurium or pancuronium.52 147

• Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.1

• Importance of informing clinician of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses (e.g., cardiovascular disease, neuromuscular disease).1

• Importance of informing patients of other important precautionary information.1 (See Cautions.)

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name