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KEY POINTS

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KEY POINTS

  1. Muscle response to stimulation can be measured clinically by acceleromyography and direct palpation.

  2. Commonly used patterns of stimulation are a single twitch, train of four, double burst, tetanic, and posttetanic count.

  3. Succinylcholine, a depolarizing neuromuscular blocking drug (NMBD), is metabolized by plasma cholinesterase. Atypical pseudocholinesterases cannot metabolize pseudocholinesterase at a normal rate, and prolonged neuromuscular blockade may result.

  4. Immobility, prolonged use of NMBDs, and upper and lower motor neuron disease may cause a proliferation of extrajunctional receptors. These receptors cause severe hyperkalemia when stimulated with succinylcholine.

  5. Nondepolarizing NMBDs are benzylisoquinoline (mivacurium, atracurium, cisatracurium) and steroidal molecules (vecuronium, rocuronium, pancuronium).

  6. The degradation of atracurium, cisatracurium, and mivacurium is independent of organ-specific elimination.

  7. Pancuronium and vecuronium are metabolized in the liver to derivatives that are cleared by the kidney and that exhibit neuromuscular blocking activities. These derivatives accumulate with prolonged administration and renal insufficiency.

  8. Reversal agents increase the concentration of acetylcholine in the junctional clefts to compete with the NMBDs to restore muscle activity.

  9. Clinical criteria, in addition to evoked responses, should be used to assess the recovery of neuromuscular blockade.

  10. Residual neuromuscular blockade is a persistent and common clinical and economic problem.

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INTRODUCTION

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Muscle relaxation can be achieved by direct central nervous system depression with volatile inhalation anesthetics or by neural blockade either at the peripheral nerve or with drugs that act at the neuromuscular junction. Neuromuscular blocking drugs (NMBDs) are essential in anesthetic practice to facilitate tracheal intubation and provide optimum surgical conditions for a variety of procedures. The use of NMBDs significantly reduces the concentration of inhalational anesthetics required to provide an appropriate depth of analgesia and amnesia. NMBDs have no inherent analgesic or amnestic properties, and their use is contraindicated if artificial ventilation is not possible.

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HISTORICAL PERSPECTIVE

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In 1850, Pelouze and Bernard demonstrated that curare, the arrow poison used by certain South American Indian tribes, abolished the effect of nerve stimulation on muscle but did not affect the excitability of either nerve or muscle. Curare and nicotine were thought to act directly on muscle through “receptive substances” rather than by action on axonal endings until stimulation of the vagus nerve was demonstrated to produce a substance, later identified as acetylcholine (ACh), which acts as a transmitter at the myoneural junction of voluntary muscle.

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CELL BIOLOGY OF MUSCLE CONTRACTION

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BASIC MYONEURAL STRUCTURE

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A motor unit is a series of muscle fibers that is innervated by the same motor nerve.1,2 The motor nerve enters skeletal muscle and ramifies to an extent that depends on the precise function of the specific muscle. The exquisite control of extraocular muscles is accomplished through a single neuron innervating one muscle fiber, in contrast to muscles that contract for more coarse activities (eg, maintenance of posture) that involve the innervation of multiple fascicles by a ...

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