Upper Airway Collapsibility during Dexmedetomidine and Propofol Sedation in Healthy Volunteers: A Nonblinded Randomized Crossover Study
Åse Lodenius, M.D., Ph.D., D.E.S.A.; Kathleen J. Maddison, Ph.D.; Brad K. Lawther, M.D.; Mika Scheinin, M.D., Ph.D.; Lars I. Eriksson, M.D., Ph.D., F.R.C.A.; et al Peter R. Eastwood, Ph.D.; David R. Hillman, M.B.B.S.; Malin Jonsson Fagerlund, M.D., Ph.D., D.E.S.A.; Jennifer H. Walsh, M.Sc., Ph.D
 Author Notes
From the Function Perioperative Medicine and Intensive Care, Karolinska University Hospital, and the Department of Physiology and Pharmacology, Section for Anesthesiology and Intensive Care, Karolinska Institutet, Stockholm, Sweden (A.L., L.I.E., M.J.F.); the West Australian Sleep Disorders Research Institute, Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia (K.J.M., P.R.E., D.R.H., J.H.W.); the Centre for Sleep Science, School of Human Sciences (K.J.M., P.R.E., D.R.H., J.H.W.) and the Department of Anaesthesia, Sir Charles Gairdner Hospital (B.K.L.), Nedlands, Western Australia, Australia; and the Institute of Biomedicine, University of Turku, and Unit of Clinical Pharmacology, Turku University Hospital, Turku, Finland (M.S.).
Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are available in both the HTML and PDF versions of this article. Links to the digital files are provided in the HTML text of this article on the Journal’s Web site (www.anesthesiology.org).
Submitted for publication October 8, 2018. Accepted for publication June 11, 2019.
Part of the work presented in this article has been presented at the Upper Airway Symposium in Clare Valley, South Australia, Australia, February 7–9, 2018 and at the Australasian Sleep Association Annual Scientific Meeting in Brisbane Australia, October 17–20, 2018.
Correspondence: Address correspondence to Dr. Lodenius: DESA, Remeo, R-kliniken AB, Thorsten Levenstams väg 4, 128 64 Sköndal, Sweden. Ase.Lodenius@remeoclinic.se. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Anesthesiology Newly Published on August 8, 2019. doi:10.1097/ALN.0000000000002883
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Abstract
Editor’s Perspective:

What We Already Know about This Topic:

Dexmedetomidine is a relatively new sedative promoted as having minimal effect on ventilatory drive or the propensity to upper airway obstruction

What This Article Tells Us That Is New:

At comparable levels of light to moderate sedation, dexmedetomidine and propofol exhibit similar degrees of pharyngeal collapsibility and reductions in ventilatory drive

The findings suggest that sedation with dexmedetomidine does not offer inherent protection against upper airway obstruction or ventilatory depression

Background: Dexmedetomidine is a sedative promoted as having minimal impact on ventilatory drive or upper airway muscle activity. However, a trial recently demonstrated impaired ventilatory drive and induction of apneas in sedated volunteers. The present study measured upper airway collapsibility during dexmedetomidine sedation and related it to propofol.

Methods: Twelve volunteers (seven female) entered this nonblinded, randomized crossover study. Upper airway collapsibility (pharyngeal critical pressure) was measured during low and moderate infusion rates of propofol or dexmedetomidine. A bolus dose was followed by low (0.5 μg · kg−1 · h−1 or 42 μg · kg−1 · min−1) and moderate (1.5 μg · kg−1 · h−1 or 83 μg · kg−1 · min−1) rates of infusion of dexmedetomidine and propofol, respectively.

Results: Complete data sets were obtained from nine volunteers (median age [range], 46 [23 to 66] yr; body mass index, 25.4 [20.3 to 32.4] kg/m2). The Bispectral Index score at time of pharyngeal critical pressure measurements was 74 ± 10 and 65 ± 13 (mean difference, 9; 95% CI, 3 to 16; P = 0.011) during low infusion rates versus 57 ± 16 and 39 ± 12 (mean difference, 18; 95% CI, 8 to 28; P = 0.003) during moderate infusion rates of dexmedetomidine and propofol, respectively. A difference in pharyngeal critical pressure during sedation with dexmedetomidine or propofol could not be shown at either the low or moderate infusion rate. Median (interquartile range) pharyngeal critical pressure was −2.0 (less than −15 to 2.3) and 0.9 (less than −15 to 1.5) cm H2O (mean difference, 0.9; 95% CI, −4.7 to 3.1) during low infusion rates (P = 0. 595) versus 0.3 (−9.2 to 1.4) and −0.6 (−7.7 to 1.3) cm H2O (mean difference, 0.0; 95% CI, −2.1 to 2.1; P = 0.980) during moderate infusion of dexmedetomidine and propofol, respectively. A strong linear relationship between pharyngeal critical pressure during dexmedetomidine and propofol sedation was evident at low (r = 0.82; P = 0.007) and moderate (r = 0.90; P < 0.001) infusion rates.

Conclusions: These observations suggest that dexmedetomidine sedation does not inherently protect against upper airway obstruction.