Questions
- 1.
Describe how nondepolarizing neuromuscular blocking drugs produce skeletal muscle relaxation.
- 2.
How do nondepolarizing neuromuscular blocking drugs differ from one another?
- 3.
- 4.
Describe the effects of metabolic derangements on nondepolarizing neuromuscular blockade.
- 5.
How do burns affect the use of nondepolarizing neuromuscular blocking drugs?
- 6.
How do other drugs and certain disease states affect nondepolarizing neuromuscular blockade?
A 22-year-old woman presented for abdominoplasty. Her weight was 75 kg and her height was 160 cm. Past medical history was significant for seizure disorder treated with phenytoin 100 mg twice daily. She had been seizure-free for the past 6 years. She had never received anesthesia before. Her plasma phenytoin level was within therapeutic range. After placement of monitors, fentanyl 100 μg and midazolam 2 mg were administered. General anesthesia was induced with propofol 200 mg, followed by vecuronium 8 mg for neuromuscular blockade. Intubating conditions were excellent. Anesthesia was maintained with isoflurane 2% in 70% oxygen/30% nitrous oxide. The end-tidal isoflurane concentration was 1.2%. During preparation of the abdomen 10 minutes later, she moved. Bispectral index was 45. Train-of-four stimulation of the ulnar nerve at the wrist demonstrated four twitches of the adductor pollicis brevis muscle.
1
Describe how nondepolarizing neuromuscular blocking drugs produce skeletal muscle relaxation.
Nondepolarizing neuromuscular blocking drugs (NMBDs) produce relaxation of voluntary (skeletal or striated) muscles by the following mechanisms:
- •
Inhibit the effect of acetylcholine by competing with it as they bind to the alpha subunit of the nicotinic acetylcholine receptor at the postjunctional membrane
- •
Block prejunctional acetylcholine receptors at the motor nerve terminal, decreasing acetylcholine release in response to motor nerve stimulation
- •
Noncompetitively block open postjunctional acetylcholine channels
2
How do nondepolarizing neuromuscular blocking drugs differ from one another?
Although numerous NMBDs are available for clinical use, structurally they fall into one of two types: steroid-based or benzylisoquinolinium compounds. Steroidal NMBDs include rocuronium, vecuronium, pancuronium, and pipecuronium. Benzylisoquinolinium compounds include atracurium, cisatracurium, mivacurium (no longer available in the United States), and doxacurium. NMBDs are usually classified according to their durations of action as short-acting, intermediate-acting, or long-acting ( Table 21-1 ). The choice of NMBDs depends on several factors, including onset time, duration of action, elimination time, potency, and route or routes of elimination. In addition, some NMBDs may have desirable or undesirable effects on the cardiovascular and respiratory systems. These effects may be mediated by the autonomic nervous system or histamine receptors or both.
| Drug | ED 95 (mg/kg) | Onset Time/Clinical RI 25–75 (min) | Elimination Half-Life * (min) | Route(s) of Elimination | Cardiovascular Effects | Histamine Release | Autonomic Ganglion Block | Intubating Dose (mg/kg) |
|---|---|---|---|---|---|---|---|---|
| Atracurium | 0.2 | Slow/11–23 | 20 | Nonenzymatic ester hydrolysis Hoffman elimination | None | Skin flushing Hypotension Bronchospasm | None | 0.5–0.6 |
| Cisatracurium | 0.05 | Slow/11–23 | 20 | Nonenzymatic ester hydrolysis Hoffman elimination | None | None | None | 0.15–0.2 |
| Mivacurium | 0.07 | Slow/6–8 | 18 | Hydrolysis by plasma cholinesterase | None | Yes | None | 0.2–0.25 |
| Pancuronium | 0.07 | Slow/24 | 145 | Renal; some hepatic | Tachycardia | None | None | 0.08–0.12 |
| Rocuronium | 0.3 | Rapid/10–15 | 60–75 | Hepatic; some renal | None | None | None | 0.6–1; 1.2 (RSI) |
| d-Tubocurarine | 0.5 | Slow/25–35 | 80 | Renal; minimal hepatic | Hypotension Bradycardia | Skin flushing | Yes | 0.5–0.6 |
| Vecuronium | 0.05 | Slow/10–15 | 62 | Hepatic; some renal | None | None | None | 0.1–0.2 |
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