Cardiovascular drugs
The anticholinergic drugs
While
numerous anticholinergic drugs exist, in anesthesia we deal almost exclu-sively
with atropine and glycopyrrolate, and occasionally with scopolamine. All three
drugs act on the autonomic nervous system, blocking the effect of
acetyl-choline at post-ganglionic nerve endings. Thus, they accelerate heart
rate (if sym-pathetic tone is present and capable of accelerating heart rate),
bronchodilate, cause mydriasis (thereby increasing intraocular pressure),
inhibit salivation (and in the process dry secretions in the upper airway),
inhibit sweating (by block-ing the effect of postganglionic sympathetic
cholinergic stimulation), and exert a variety of effects on the GI and GU
systems. In anesthesia we use atropine or glycopyrrolate to counteract
bradycardia, salivation, and intestinal cramping, all of which are side effects
of neostigmine.
Atropine
and scopolamine are tertiary amines and thus capable of crossing the
blood–brain barrier. In the elderly, scopolamine often causes delirium. Both
drugs cross the placenta, and atropine has been observed to accelerate fetal
heart rate. Both drugs have a dual effect – in addition to their
well-recognized peripheral anti-cholinergic effect, they have a stimulating
central vagal effect. With scopolamine, we sometimes see bradycardia when the
central stimulating effect outlasts the peripheral blocking effect of the drug.
Glycopyrrolate is a quaternary, charged compound and thus largely prevented
from crossing the blood–brain barrier or the placenta.
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