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Updated: Oct 17 2021

Neuromuscular Blockade

  • Snapshot
    • A 46-year-old woman is undergoing an elective roux-en-y gastric bypass procedure to manage her obesity. The anesthesiology resident begins to induce anesthesia in the patient, which involved providing succinylcholine. After administration of this depolarizing agent, she developed fasciculations that eventually ceased.
  • Introduction
    • Neuromuscular blockade
      • clinical use
        • an agent used to provide muscle relaxation and diminish reflexes
          • this is useful for tracheal intubation and surgery
      • mechanism of action
        • impairs cholinergic transmission at the neuromuscular junction
          • which is accomplished by certain neuromuscular blocking agents being
            • nicotinic receptor antagonists
              • these are classified as non-depolarizing agents
            • nicotinic receptor agonists
              • these are classified as depolarizing agents
    • Non-depolarizing neuromuscular blockers
      • medications
        • atracurium, mivacurium, pancuronium, rocuronium, tubocurarine, and vecuronium
      • mechanism of action
        • competes with acetylcholine for binding of nicotinic receptors on the motor-end plate
          • this prevents depolarization and thus inhibiting muscle contraction
          • therefore, reversed by increasing the acetylcholine concentration in the neuromuscular junction with acetylcholinesterase inhibitors (e.g., neostigmine)
            • overcomes the antagonistic effect of these non-depolarizing agents
            • administer with atropine to prevent off-target muscarinic effects
    • Depolarizing neuromuscular blockers
      • medication
        • succinylcholine
      • mechanism of action
        • binds to nicotinic receptors; however, they are more resistant to acetylcholinesterases than acetylcholine
          • therefore, they provide constant stimulation of the receptor
            • phase I depolarization
              • prolonged depolarization at the receptor
                • there is no antidote and block is potentiated by acetylcholinesterase inhibitors
                  • paradoxical, but acetylcholinesterase inhibitors may inhibit other cholinesterases that do break down succinylcholine (e.g., pseudocholinesterase)
                • can manifest as fasciculations
            • phase II depolarization
              • repolarization, thus making the receptor unable to transmit further electrical impulses
                • antidote
                  • acetylcholinesterase inhibitors
      • adverse effects
        • malignant hyperthermia
        • hyperkalemia
          • especially in burn patients or those with extensive tissue damage
          • denervating neuromuscular diseases (e.g., ALS or MS) secondary to upregulation of ACh receptors
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