Effects of dexmedetomidine and propofol on the key endotypes of OSA: A randomized, single-blind, placebo-controlled, crossover trial.

BACKGROUND

Drug-induced sleep has been shown to facilitate the diagnosis of obstructive sleep apnea (OSA). However, the effects of commonly used sedatives, such as dexmedetomidine and propofol, on the endotypic traits of OSA remained unclear.

OBJECTIVE

We aim to investigate the impact of dexmedetomidine and propofol on OSA endotypic traits.

METHODS

We conducted a randomized, single-blind, placebo-controlled, crossover trial in adult patients with OSA, comparing the OSA endotypic traits and polysomnography parameters among the interventions of placebo, dexmedetomidine and propofol.

RESULTS

16 patients completed the trial and were enrolled for analysis. Both dexmedetomidine and propofol worsened pharyngeal collapsibility as indicated by a lower Vpassive (mean difference: 6.1 [95 % CI -9.1 to -3.0]%eupnea for dexmedetomidine versus placebo, p = 0.040; -16.5 [95 % CI -24.1 to -9.0]%eupnea for propofol versus placebo, p < 0.001), with propofol causing a greater effect (-10.4 [95 % CI -17.8 to -3.2]%eupnea for propofol versus dexmedetomidine, p < 0.001). Dexmedetomidine maintained upper airway gain, while propofol diminished it compared to placebo (p = 0.001). Both dexmedetomidine and propofol increased arousal threshold (p = 0.006 and p < 0.001, respectively). Dexmedetomidine had no effect on loop gain, whereas propofol elevated it (p = 0.004). Compared to placebo, dexmedetomidine had no impact on apnea-hypopnea index (AHI) or saturation of peripheral oxygen (SpO2). During propofol sedation, AHI in stages N1 (p < 0.001), N2 (p < 0.001) and the entire NREM (p = 0.038) sleep showed increases, and nadir SpO2 for NREM stage exhibited a decrease (p = 0.006).

CONCLUSIONS

Dexmedetomidine had less impact on OSA endotypic traits compared to propofol, and had no negative effects on AHI and SpO2.