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Neostigmine respiratory effects

C. Atropine will not directly paralyze the respiratory muscles. However, it can prevent the detection of early signs of an overdose of neostigmine, which can quickly progress to a depolarizing block of skeletal muscle and paralysis of the respiratory muscles. Dry mouth, ocular disturbances, and tachycardia are common side effects of atropine given alone, but these effects are less likely to occur with competition between atropine and the increase in the synaptic ACh produced by inhibition of AChE by neostigmine. [Pg.139]

In very high doses, aminoglycosides can produce a curare-like effect with neuromuscular blockade that results in respiratory paralysis. This paralysis is usually reversible by calcium gluconate (given promptly) or neostigmine. Hypersensitivity occurs infrequently. [Pg.1023]

Interactions. Morphine (also pethidine and possibly other opioids) is potentiated by monoamine oxidase inhibitors. Any central nervous system depressant (including alcohol) will have additive effects. Patients recently exposed to neuromuscular blocking agents (unless this is adequately reversed, e.g. by neostigmine) are particularly at risk from the respiratory depressant effects of morphine. The effect of diuretic drugs may be reduced by release of antidiuretic hormone by morphine. Useful interactions include the potientating effect on pain relief of tricyclic antidepressants and of dexamfetamine. [Pg.336]


See other pages where Neostigmine respiratory effects is mentioned: [Pg.127]    [Pg.136]    [Pg.187]    [Pg.178]    [Pg.2492]    [Pg.178]    [Pg.350]    [Pg.578]    [Pg.375]    [Pg.438]    [Pg.248]    [Pg.120]    [Pg.128]    [Pg.132]    [Pg.480]   
See also in sourсe #XX -- [ Pg.393 ]




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