Muscle response to stimulation can be measured by mechanomyography, electromyography, acceleromyography, and direct palpation.
Commonly used patterns of stimulation are a single twitch, train of four, double burst, tetanic, and posttetanic count.
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.
Immobility, prolonged use of NMBDs, and upper and lower motor neuron disease may cause a proliferation of extrajunctional receptors. These receptors affect severe hyperkalemia when stimulated with succinylcholine.
Nondepolarizing NMBDs are benzylisoquinoline (mivacurium, atracurium, cisatracurium) and steroidal molecules (vecuronium, rocuronium, pancuronium).
The degradation of atracurium, cisatracurium, and mivacurium is independent of organ-specific elimination.
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.
Reversal agents increase the concentration of acetylcholine in the junctional clefts to compete with the NMBDs to restore muscle activity.
Clinical criteria, in addition to evoked responses, should be used to assess the recovery of neuromuscular blockade.
Residual neuromuscular blockade is a persistent and common clinical problem.
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 (NMBD) are essential in anesthetic practice to facilitate tracheal intubation and provide optimum surgical conditions for a variety of procedures. The use of NMBDs is to significantly reduce the concentration of volatile anesthetics required to provide adequate analgesia. NMBDs have no inherent analgesic or amnestic properties, and their use is contraindicated if artificial ventilation is not possible.
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), as transmitter at the myoneural junction of voluntary muscle.
Basic Myoneural Structure
A motor unit is a series of muscle fibers that is innervated by the same motor nerve.1 This nerve enters skeletal muscle and ramifies to an extent that depends on the function of the specific muscle. For example, each muscle fiber of an extraocular eye muscle is innervated by a single neuron. In contrast, muscles that contract for more coarse activities (eg, maintenance of posture) have multiple fascicles that are innervated by a single nerve fiber.
Stimulation of a single motor nerve leads to contraction of all the muscle fibers contained within the particular motor unit. As the axons terminate in troughs on the surface of the muscle fibers, their ...