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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.