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induced by ketamine’s propensity to increase salivary secretions should be considered when using this sedative in oral regimens. In addition, some settings and regions may prohibit its use by personnel not trained in the administration and management of deep sedation or general anesthesia. Zolpidem Zolpidem is a short-acting “nonbenzodiazepine” hypnotic drug colloquially referred to as a member of the “Z-drug” family along with zopiclone and zaleplon. Binding still occurs on the GABA A receptor similarly to benzodiazepines; however

α1 subunit (BZ 1 receptor) described above which putatively reduces their potential for cognitive impairment and abuse. 46 Whether these claims actually bear fruit remains to be seen. Zolpidem (Ambien) Unlike the benzodiazepines, zolpidem produces muscle relaxation and anticonvulsant effects only at doses much higher than the hypnotic dose. 47 Zolpidem has a rapid onset of action, usually within 30 minutes, has a short elimination half-life and no active metabolites. This reduces the possibility of residual next-day effects from

may feel fully recovered. Interestingly, 2 of the patients who took triazolam required a full night’s sleep to return to normal function. This is concerning in light of recent recommendations by some groups to use much higher and multiple doses of triazolam for dental office sedation. Both agents were similar in regard to relief of anxiety when using a self-reported VAS. This is important since the nonbenzodiazepine GABA A agonists, such as zaleplon and zolpidem (Ambien), may have differential effects on central nervous system GABA receptors such that

, 34.1 kg/m 2 ) was scheduled for dental treatment and removal of a lower third molar under general anesthesia at our institution. She had severe mental retardation and required assistance in everyday life. The patient exhibited no understanding of verbal communication. Because of cognitive impairment, we were unable to perform a complete preoperative airway assessment. She had no problems associated with eating or apparent mouth opening, however. She was taking diazepam for epilepsy and brotizolam and zolpidem for insomnia. No other abnormalities that would have

normal dose range. When triazolam was originally developed, the FDA approved marketing of a 0.5 mg tablet, but because of postmarketing reports of significant side effects at that dose, the 0.5 mg tablet was eliminated in favor of the lower dosage forms currently available. Similarly, the FDA recently has decreased the MRD for zolpidem (Ambien), a drug for insomnia that is similar to triazolam, although it is in a slightly different class. The FDA has now indicated that the 10-mg dose recommendation should be decreased to 5 mg in women, and the prescriber

account for subtle differences in the range of effects provided by a particular benzodiazepine. Already the so-called nonbenzodiazepines or “Z-compounds” such as zolpidem (Ambien) are claimed as more selective BZ 1 agonists and are promoted for treatment of insomnia. All benzodiazepines exhibit comparable efficacy as sedatives. In addition to their sedative effects, they also produce varying degrees of anterograde amnesia. Once recovered, patients have difficulty recalling events that occurred while they were sedated. It is significant that the patient

triazolam (Halcion) and zolpidem (Ambien). 10 Figure 7. Onset and duration of sedation. Following absorption, serum concentrations are high and drug distributes to tissues in proportion to their degree of perfusion; brain, muscle, and finally adipose tissues. As distribution proceeds, serum level declines and high concentrations in brain redistribute into the bloodstream. These processes occur more rapidly with highly lipid soluble drugs and account for rapid onset but shortened duration of sedation. Drug elimination follows

medications included alprazolam, aspirin, atorvastatin, cyclobenzaprine, empagliflozin, folic acid, insulin glargine, lisinopril, metformin, pioglitazone, repaglinide, and zolpidem. The patient reported negative personal and family history of adverse reactions to anesthesia and indicated no known drug allergies. He also reported quitting cigarette smoking approximately 3 weeks prior to the surgery date. Physical examination revealed full range of motion of the neck and a Mallampati class II airway. Inspection of the oral cavity and oropharynx was unremarkable. Auscultation

of CRPS type I following injury to her right forearm as detailed below. Her medications included zolpidem (10 mg every evening at bedtime [qhs]), lorazepam (1 mg as needed [prn] for anxiety) and acetaminophen/oxycodone (325 mg/10 mg, 2 tablets prn pain). She reported an allergy to haloperidol that caused “a swollen tongue and difficulty swallowing.” Past surgical history included ankle surgery prior to the arm injury with no anesthetic complications and third molar extraction with CRPS flare up. The patient had undergone multiple ketamine infusions, local

more traditional benzodiazepines. These newer agents include zolpidem (Ambien) and Zaleplon (Sonata), having relatively fast onset and short durations, and eszopiclone (Lunesta) having a slower onset and longer duration. Dental Implications for Patients Medicated with Sedative-Anxiolytics Drug tolerance and dependence are the principal concerns for the dentist when managing patients taking sedatives chronically. Common sense dictates caution when administering sedation or general anesthesia due to the potential for enhanced CNS