Editorial Views  |   November 2019
Dexmedetomidine and the Upper Airway: Not as Simple as We Hoped
Author Notes
  • From the University of Rochester Medical Center, University of Rochester School of Medicine and Dentistry, Rochester, New York (D.S.W., S.B.K.); Maine Medical Center, Portland, Maine (D.S.W.); and Tufts University School of Medicine, Boston, Massachusetts (D.S.W.).
  • This editorial accompanies the article on p. 962.
    This editorial accompanies the article on p. 962.×
  • Accepted for publication August 6, 2019.
    Accepted for publication August 6, 2019.×
  • Address correspondence to Dr. Ward: Denham_Ward@URMC.Rochester.edu
Article Information
Editorial Views / Pharmacology / Respiratory System
Editorial Views   |   November 2019
Dexmedetomidine and the Upper Airway: Not as Simple as We Hoped
Anesthesiology 11 2019, Vol.131, 953-954. doi:10.1097/ALN.0000000000002965
Anesthesiology 11 2019, Vol.131, 953-954. doi:10.1097/ALN.0000000000002965
With the epidemic of obstructive sleep apnea syndrome, concern about airway obstruction during sedation has increased. Dexmedetomidine, used for sedation in the intensive care unit and during procedures, has been thought to have fewer respiratory depressive effects than other sedatives, although airway obstructions and apneas with dexmedetomidine have been noted in several studies.2,3  This issue of Anesthesiology features work by Lodenius et al.,4  who found that dexmedetomidine is not superior to propofol in the propensity for causing airway obstruction at comparable sedation levels.
Sedative agents depress ventilation through a variety of actions including direct actions on upper airway muscle tone,5  on chemosensory pathways, and by removal of the “wakefulness” drive.6  Loss of the wakefulness input can unmask a profound depression of the chemosensory drive from sedatives and analgesics7  and reduce the drive to the pharyngeal dilator muscles. Respiratory physiologists routinely discriminate new sedative and opioid agents by their effects on the depression of the hypoxic and hypercapnic chemosensitivity.8  Moderate depression of the chemoreflexes is well tolerated, particularly when supplemental oxygen is supplied. However, even with supplemental oxygen, upper airway obstruction may result in serious hypoxemia in a matter of minutes. In sleep apnea research, the collapsibility of the upper airway during sleep has been quantified by the estimation of the pharyngeal pressure that is required to close the airway or keep it open.9,10  This methodology is being used to assess the propensity of medications to increase airway collapsibility.