scholarly journals Upper Airway Collapsibility during Dexmedetomidine and Propofol Sedation in Healthy Volunteers: A Nonblinded Randomized Crossover Study: Erratum

2020 ◽  
Vol 132 (3) ◽  
pp. 602-602
2019 ◽  
Vol 131 (5) ◽  
pp. 962-973 ◽  
Author(s):  
Åse Lodenius ◽  
Kathleen J. Maddison ◽  
Brad K. Lawther ◽  
Mika Scheinin ◽  
Lars I. Eriksson ◽  
...  

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New 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.


2011 ◽  
Vol 115 (2) ◽  
pp. 273-281 ◽  
Author(s):  
Masato Kobayashi ◽  
Takao Ayuse ◽  
Yuko Hoshino ◽  
Shinji Kurata ◽  
Shunji Moromugi ◽  
...  

Background Head elevation can restore airway patency during anesthesia, although its effect may be offset by concomitant bite opening or accidental neck flexion. The aim of this study is to examine the effect of head elevation on the passive upper airway collapsibility during propofol anesthesia. Method Twenty male subjects were studied, randomized to one of two experimental groups: fixed-jaw or free-jaw. Propofol infusion was used for induction and to maintain blood at a constant target concentration between 1.5 and 2.0 μg/ml. Nasal mask pressure (PN) was intermittently reduced to evaluate the upper airway collapsibility (passive PCRIT) and upstream resistance (RUS) at each level of head elevation (0, 3, 6, and 9 cm). The authors measured the Frankfort plane (head flexion) and the mandible plane (jaw opening) angles at each level of head elevation. Analysis of variance was used to determine the effect of head elevation on PCRIT, head flexion, and jaw opening within each group. Results In both groups the Frankfort plane and mandible plane angles increased with head elevation (P < 0.05), although the mandible plane angle was smaller in the free-jaw group (i.e., increased jaw opening). In the fixed-jaw group, head elevation decreased upper airway collapsibility (PCRIT ~ -7 cm H₂O at greater than 6 cm elevation) compared with the baseline position (PCRIT ~ -3 cm H₂O at 0 cm elevation; P < 0.05). Conclusion : Elevating the head position by 6 cm while ensuring mouth closure (centric occlusion) produces substantial decreases in upper airway collapsibility and maintains upper airway patency during anesthesia.


SLEEP ◽  
2011 ◽  
Vol 34 (6) ◽  
pp. 717-724 ◽  
Author(s):  
Helena Larramona Carrera ◽  
Joseph M. McDonough ◽  
Paul R. Gallagher ◽  
Swaroop Pinto ◽  
John Samuel ◽  
...  

1990 ◽  
Vol 141 (6) ◽  
pp. 1569-1577 ◽  
Author(s):  
Michael J. Wasicko ◽  
Douglas A. Hutt ◽  
Richard A. Parisi ◽  
Judith A. Neubauer ◽  
Reuben Mezrich ◽  
...  

2016 ◽  
Vol 48 (5) ◽  
pp. 1340-1350 ◽  
Author(s):  
Luigi Taranto-Montemurro ◽  
Scott A. Sands ◽  
Bradley A. Edwards ◽  
Ali Azarbarzin ◽  
Melania Marques ◽  
...  

We recently demonstrated that desipramine reduces the sleep-related loss of upper airway dilator muscle activity and reduces pharyngeal collapsibility in healthy humans without obstructive sleep apnoea (OSA). The aim of the present physiological study was to determine the effects of desipramine on upper airway collapsibility and apnoea–hypopnea index (AHI) in OSA patients.A placebo-controlled, double-blind, randomised crossover trial in 14 OSA patients was performed. Participants received treatment or placebo in randomised order before sleep. Pharyngeal collapsibility (critical collapsing pressure of the upper airway (Pcrit)) and ventilation under both passive (V′0,passive) and active (V′0,active) upper airway muscle conditions were evaluated with continuous positive airway pressure (CPAP) manipulation. AHI was quantified off CPAP.Desipramine reduced activePcrit(median (interquartile range) −5.2 (4.3) cmH2O on desipramineversus−1.9 (2.7) cmH2O on placebo; p=0.049) but not passivePcrit(−2.2 (3.4)versus−0.7 (2.1) cmH2O; p=0.135). A greater reduction in AHI occurred in those with minimal muscle compensation (defined asV′0,active−V′0,passive) on placebo (r=0.71, p=0.009). The reduction in AHI was driven by the improvement in muscle compensation (r=0.72, p=0.009).In OSA patients, noradrenergic stimulation with desipramine improves pharyngeal collapsibility and may be an effective treatment in patients with minimal upper airway muscle compensation.


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