RT Book, Section A1 Pino, Richard M. A1 Ali, Hassan H. A2 Longnecker, David E. A2 Mackey, Sean C. A2 Newman, Mark F. A2 Sandberg, Warren S. A2 Zapol, Warren M. SR Print(0) ID 1144116340 T1 Monitoring and Managing Neuromuscular Blockade T2 Anesthesiology, 3e YR 2017 FD 2017 PB McGraw-Hill Education PP New York, NY SN 9780071848817 LK accessanesthesiology.mhmedical.com/content.aspx?aid=1144116340 RD 2024/04/24 AB KEY POINTSMuscle response to stimulation can be measured clinically by 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 cause 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 and economic problem.