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Patients who overdose on sympathomimetic agents exhibit a syndrome of excess adrenergic tone due to direct stimulation of adrenergic receptors or the effects of norepinephrine and epinephrine. Many of the agents in this category are drugs of abuse, although several therapeutic agents can produce a similar toxidrome.
Agents that fall into this category include amphetamines, cocaine, vasopressors, methylxanthines, synthetic cannabinoids and cathinones, and β-agonists.
Stimulants and street drugs were the ninth most common human exposure in adults but were the third leading cause of fatal exposures according to the AAPCC in 2016.1
- Agents that stimulate the SNS generally do so by either causing the release or preventing the reuptake of endogenous catecholamines or directly stimulating α- and/or β-receptors.
- Methylxanthines (theophylline, caffeine) and β-agonists (albuterol, dobutamine, isoproterenol) enhance chronotropy and inotropy by facilitating calcium entry into the myocardium. They also enhance the function of β2-receptors leading to bronchodilatation. Stimulation of the β2-rich vascular beds to skeletal muscle results in vasodilatation as well. Therefore, in a pure β-agonist overdose, hypotension and tachycardia predominate.
- Epinephrine, norepinephrine, cocaine, and amphetamines have both α and β effects, resulting in hypertension and tachycardia.
- Other α-receptors are found on the iris, which, when stimulated, results in pupillary dilatation.
- Sympathetic stimulation of sweat glands is a cholinergic effect.
- Synthetic cannabinoids act on the cannabinoid receptors but may result in sympathomimetic effects.2