**2. Beta-blocker therapy in acute stimulant toxicity**

Current literature recommends against the use of beta-blockers in the setting of cocaine-induced-chest-pain. Small catheter-based-human-studies and case reports have suggested they might exacerbate coronary vasospasm and the toxic effects of cocaine by inducing "unopposed" alpha-adrenergic stimulation [1–3]. Two high quality systematic clinical reviews have demonstrated lack of evidence preventing the use of BBT in both acute methamphetamine and cocaine intoxication. Findings show the superiority of beta-blockers in the management of both stimulant-induced HTN and tachycardia when compared to first-line treatment choices calcium-channel blockers and nitrates; which were shown to only attenuate HTN and not tachycardia [1, 2].

The most recent 2012 ACCF/AHA guidelines endorse the use of labetalol (nonselective with alpha-properties) in acute stimulant toxicity given certain vital sign parameters and only after a vasodilator is given prior. These guidelines also endorse there is a lack of literature investigating these effects in methamphetamine users; and currently recommend that treatment for acute methamphetamine toxicity the same as cocaine toxicity pending future investigation [5].

Current evidence shows that providers have been using BBT during acute stimulant toxicity without causing any adverse cardiac events [1, 2, 6]. For instance, a retrospective study examined 376 patients presenting to the emergency department (ED) with acute coronary syndrome (ACS) and self-reported cocaine use within 24-hours in the presence of positive urine drug screen (UDS) for cocaine. Betablockers given were metoprolol (45%), carvedilol (26%), labetalol (27%), or atenolol (2%). No differences were found between selective, non-selective beta-blockers, rate of death, stroke or arrhythmia compared to those not receiving BBT [6]. These findings demonstrate that it is safe to implement BBT during the management of patients presenting with ACS secondary to acute cocaine intoxication.

A systematic review and meta-analysis of five studies were performed involving 1794 patients presenting with cocaine-associated-chest-pain (CACP). The authors found no increased risk of non-fatal MI or all-cause mortality in patients given BBT versus no BBT [7]. This evidence supports the idea that BBT is safe in patients experiencing concomitant stimulant toxicity. This same idea can be applied to the use of long-term BBT. If BBT is safe in acute toxicity then it should demonstrate safety in patients who are prescribed beta-blockers daily who also abuse cocaine or methamphetamine.
