Limited analgesic and respiratory effects
Wide variation in efficacy (genetic variation in demethylation ability)
CMRO2, cerebral metabolic rate for oxygen; CBF, cerebral blood flow; ICP, intracranial pressure; CPP, cerebral perfusion pressure
CMRO2, cerebral metabolic rate for oxygen; CBF, cerebral blood flow; ICP, intracranial pressure; CPP, cerebral perfusion pressure owing to leakage of intracellular potassium. Where sodium-potassium channel populations increase (following burns, denervation, crush injury or tetanus), potassium release may be catastrophic. Approximately 1 : 3,000 of patients given succinylcholine fail to metabolize the drug normally. This may lead to prolonged (several hours) paralysis, the so-called "Anectine apnea". The effect of succinylcholine on ICP and CBF is controversial. There is evidence that succinylcholine can cause an increase in ICP in individuals with compromised intracranial compliance . This may be because the increased muscle spindle activity resulting from fasciculation causes increased cerebral afferent input and increases CBF. Many different stimuli that affect CBF and ICP occur at the time of induction of anesthesia when succinylcholine is given, and it is likely that the effect of succinyl-choline on ICP is relatively unimportant in the clinical setting. It can be abolished by pre-treatment with a non-depolarizing neuro-muscular blocker .
Non-depolarizing muscle relaxants competitively block the action of acetylcholine at the neuromuscular junction. They lead to a flaccid paralysis and can be displaced from the acetyl choline receptor by increasing the concentration of acetylcholine by the use of an anticholinesterase (neostigmine). Earlier introduced agents of this group have side-effects such as histamine release or sympathetic stimulation. Atracurium, cisatracurium and mivac-urium are broken down to inactive metabolites in the plasma and can be used without prolonged effect in patients with renal failure .
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