In the past, atropine and defasciculating doses of nondepolarizing neuromuscular blocking agents (NMBAs) were considered mainstays of premedication. Theorized to prevent reflex bradycardia seen in the pediatric population, atropine was dosed at 0.02 mg/kg IV. A 2007 review article in Emergency Medicine Journal reevaluating the use of atropine in pediatric RSI revealed that no evidence supports the routine use of atropine to decrease the incidence of bradycardia.⁵ Further, atropine complicates an already high-stress environment of pediatric RSI, while also having the potential to induce dysrhythmias. Atropine has now fallen out of favor as a pretreatment agent.¹

Defasciculating doses of a nondepolarizing NMBA were used to prevent the theoretical rise in ICP created by fasciculations caused by succinylcholine use. Classically, rocuronium, vecuronium, or pancuronium were administered at one-tenth of the paralytic dose. A randomized, controlled trial showed no differences in fasciculations in head-injured patients when comparing pretreatment with pancuronium versus pretreatment with mini-dose succinylcholine when paralyzing with succinylcholine. The ultimate conclusion is that succinylcholine alone is an acceptable intubating agent in head-injured patients.⁶ Further, a literature review by Clancy and colleagues in Emergency Medicine Journal found no definitive evidence that succinylcholine causes a rise in ICP.⁷ Evidence does not suggest that succinylcholine worsens outcomes in at-risk patients, nor does evidence suggest that defasciculation improves outcomes in at-risk patients. Currently, defasciculation is no longer recommended.¹

Sedation

After premedication, sedation is the next step in RSI pharmacology. This step allows the emergency physician to induce a state of unconsciousness and amnesia. An ideal sedative would have a rapid onset of action, short duration, and a hemodynamically neutral profile. Unfortunately, most sedatives will cause apnea, myocardial depression, and hypotension to varying degrees. As with pretreatment agents, the emergency physician will be able to customize the sedative to the clinical circumstance (Table 1).

Because of its positive hemodynamic profile, etomidate has become the sedative of choice for RSI. Etomidate is an imidazole derivative dosed at 0.3 mg/kg IV; the time of onset is 15-30 seconds, and the duration of action is approximately 3-12 minutes.¹ Its minimal effects on blood pressure and heart rate, combined with its rapid onset, makes this drug safe in most RSI situations.⁸ Etomidate may have deleterious effects in two disease states: sepsis and seizures. During EEG monitoring, etomidate use has been shown to increase seizure activity.⁹ With other options available, etomidate should be avoided in status epilepticus.