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  1. Neuromuscular blocking drugs (NMBDs) are quaternary ammonium compounds that have structural similarities to acetylcholine (Ach).

  2. The potency of a NMBD is a measure of the dose required to produce the corresponding twitch suppression.

  3. The onset time is the time from administration to maximum blockade.

  4. The duration of action is the time to return to 25% of baseline single twitch height (T25).

  5. Succinylcholine is the only clinically available depolarizing NMBD and is hydrolyzed by plasma cholinesterase (also referred to as butyrylcholinesterase or pseudocholinesterase).

  6. The efficacy of a patient’s plasma cholinesterase can be expressed by the dibucaine number.

  7. Contraindications to succinylcholine administration include personal or family history of malignant hyperthermia, known or suspected myopathy, hyperkalemia, and medical conditions that result in increased extrajunctional acetylcholine receptors such as burns, trauma, and immobility.

  8. The routine use of succinylcholine in infants and children should be avoided due to the risk of hyperkalemic cardiac arrest in patients with undiagnosed skeletal muscle myopathy.

  9. There are two chemical classes of clinically available nondepolarizing NMBDs: the aminosteroid compounds (pancuronium, vecuronium, rocuronium) and the benzylisoquinolinium compounds (atracurium, cisatracurium, mivacurium).

  10. There are two classes of agents for reversal of neuromuscular blockade: anticholinesterases and cyclodextrins.


The neuromuscular junction consists of the prejunctional motor neuron, synaptic cleft, and postsynaptic endplate of the skeletal muscle membrane (Figure 7-1).1 Neuromuscular transmission begins when an action potential in the prejunctional motor neuron reaches the nerve terminal. The arrival of the action potential triggers the opening of voltage-gated calcium channels, leading to the influx of calcium ions. The increase in calcium results in fusion of vesicles containing acetylcholine (ACh) molecules with the membrane of the nerve terminal, thus releasing ACh into the synaptic cleft by exocytosis. ACh serves as the neurotransmitter at the neuromuscular junction and is synthesized and stored in vesicles at the motor nerve terminal.2

Figure 7-1

The neuromuscular junction. (Adapted with permission, from Widmaier EP, Raff H, Strang KT: Vander’s Human Physiology: The Mechanisms of Body Function. 11th ed. 2008. Copyright © McGraw Hill LLC. All rights reserved.)

ACh released into the synaptic cleft diffuses to the motor endplate and binds to nicotinic ACh receptors. The ACh receptor consists of five subunits arranged in a rosette to form an ion channel. The simultaneous binding of two ACh molecules to the two α subunits of the ACh receptor causes the channel to open, allowing inward movement of sodium ions and outward movement of potassium ions. The increase in intracellular sodium depolarizes the membrane, generating an action potential that propagates along the length of the muscle fiber, leading to muscular contraction. Once in the synaptic cleft, ACh is rapidly hydrolyzed by acetylcholinesterase. The motor nerve ending also reuptakes ACh.3

ACh receptors are located at prejunctional, postjunctional, and ...

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