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| Intravenous Drugs | Inhalational Drugs | Muscle Relaxants |

 

Muscle relaxants do not cross the blood-brain barrier. Any cerebral effects are thus secondary to histamine release, systemic hemodynamic changes, actions of metabolites, and altered cerebral afferent input.
 

Nondepolarizing muscle relaxants
 

Short-acting drugs. Mivacurium is a short-acting relaxant that is metabolized by plasma cholinesterase (at about 88% of the rate of succinylcholine) and undergoes ester hydrolysis in the liver. It is commonly given by infusion because of its rapid metabolism. When large doses of mivacurium are given rapidly, some histamine release can occur. Therefore, bolus doses should be given slowly over a period of 30 to 60 seconds to avoid histamine release and the potential for an increase in CBF and ICP.

Intermediate-acting drugs. Atracurium causes histamine release when given in large bolus doses. It is metabolized by ester hydrolysis and Hoffmann elimination and has an advantage in that with renal or liver dysfunction, atracurium does not alter its metabolism. Laudanosine, a metabolite of the Hoffmann elimination of atracurium, has been shown to cause seizures in laboratory animals although this has not been noted at the level obtained clinically. The newer analog of atracurium, cis-atracurium, does not cause histamine release and is not associated with the formation of toxic metabolites.
Vecuronium has the advantage of maintaining stable hemodynamics even when given in large doses. One possible exception is that bradycardia may occur when vecuronium is combined with large doses of narcotics for induction of anesthesia, leaving the vagotonic effect of the narcotic unopposed. Vecuronium does not alter ICP or CSF dynamics with no change in Vf or Ra. Its stable hemodynamics and lack of cerebral effects have made vecuronium a popular choice in neuroanesthesia.
Rocuronium is a nondepolarizing muscle relaxant that has a relatively stable hemodynamic profile (weakly vagolytic) and is excreted unchanged by the biliary system and the kidneys. Unlike vecuronium, it is not associated with the production of active metabolites. The rapid onset of rocuronium makes it an excellent choice for intubation in the neurosurgical patient who is at risk for succinylcholine side effects but in whom rapid onset of action is desirable.
 

Long-acting drugs. Pancuronium decreases the MAC of volatile anesthetics, secondary to the decrease in cerebral input from paralyzed muscle spindles. Large doses of pancuronium may cause hypertension and tachycardia, which could increase CBF and ICP. These effects may not occur when pancuronium is combined with narcotics for induction or when it is given in smaller doses for maintenance of relaxation.
Doxacurium, a long-acting muscle relaxant, is devoid of significant cardiovascular side effects and has not been shown to have any adverse cerebral effects. It is eliminated unchanged in the kidney and bile. Doxacurium's lack of side effects and long duration of action make this relaxant useful for very lengthy neurosurgical procedures.
 

Depolarizing muscle relaxants.

Succinylcholine can cause an increase in CBF that is associated with an increase in ICP. This is secondary to increases in muscle spindle activity, which increase cerebral afferent input. These effects can be blocked by prior paralysis or pretreatment with a nondepolarizing muscle relaxant. The changes in ICP are modest and transient, however, and may be outweighed by the benefit of rapid and reliable onset of muscle relaxation in instances in which rapid control of the airway is necessary. Succinylcholine produces no change in either Vf or Ra and no predicted effect on ICP. Of greater concern than succinylcholine's effect on ICP in the neurosurgical patient is the exaggerated release of potassium that occurs with certain neurologic injuries such as closed head trauma, cerebrovascular accidents, hemiparesis, spinal cord trauma, and neuromuscular disorders.


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