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.