Sympathomimetic Toxicity Medication
- Author: Paul Kolecki, MD, FACEP; Chief Editor: Asim Tarabar, MD more...
Treatment of sympathomimetic toxicity is focused on controlling agitation, managing seizure activity, and treating hypertension unresponsive to sedation. The most accepted pharmacologic option for controlling agitation is the use of benzodiazepines. Butyrophenones lower the seizure threshold, increase the risk of hyperthermia, and may prolong the QT interval (eg, droperidol); the use of butyrophenones is NOT recommended. Sympathomimetic-induced seizures should be treated with benzodiazepines or barbiturates (eg, phenobarbital). Hypertension should be managed with a short-acting, easily titrated agent (eg, nitroprusside) if it is not controlled with benzodiazepine-induced sedation.
Benzodiazepines and other sedatives
Used for controlling sympathomimetic-induced agitation.
Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.
Individualize dosage and increase cautiously to avoid adverse effects. Easily titrated with a long half-life.
Sedative hypnotic with short onset of effects and relatively long half-life.
By increasing the action of GABA, a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.
Excellent when patient requires sedation for more than 24 h.
Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.
Interferes with transmission of impulses from thalamus to cortex of brain. Used for sympathomimetic-induced seizure unresponsive to diazepam.
Control sympathomimetic-induced hypertension.
Rapidly acting, easily titrated antihypertensive. Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.
Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production, resulting in a decrease in blood pressure.
May administer bolus of 12.5-25 mcg before continuous infusion.
Initial infusion rate of 10-20 mcg/min may be increased 5-10 mcg/min q5-10min until desired clinical or hemodynamic response is achieved.
Infusion rates of 500 mcg/min have occasionally been required.
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