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Anesthetic agents inhibit the respiratory activity of upper airway muscles more than the diaphragm, creating a potential for narrowing or complete closure of the pharyngeal airway during anesthesia. Because the underlying mechanisms leading to airway obstruction in sleep apnea and during anesthesia are similar, it was hypothesized that anesthesia-induced pharyngeal narrowing could be counteracted by applying nasal continuous positive airway pressure (CPAP).Anesthesia was induced in ten healthy volunteers (aged 25-34 yr) by intravenous administration of propofol in 50-mg increments every 30-s to a maximum of 300 mg. Magnetic resonance images of the upper airway (slice thickness of 5 mm or less) were obtained in the awake state, during propofol anesthesia, and during administration of propofol plus 10 cm nasal CPAP.Minimum anteroposterior diameter of the pharynx at the level of the soft palate decreased from 6.6+/-2.2 mm (SD) in the awake state to 2.7+/-1.5 mm (P < 0.05) during propofol anesthesia and increased to 8.43+/-2.5 mm (P < 0.05) after nasal CPAP application. Anteroposterior diameter of the pharynx at the level of the dorsum of the tongue increased from 7.9+/-3.5 mm during propofol anesthesia to 12.9+/-3.6 mm (P < 0.05) after nasal CPAP. Pharyngeal volume (from the tip of the epiglottis to the tip of the soft palate, assuming this space to be a truncated cone) significantly increased from 2,437+/-1,008 mm3 during propofol anesthesia to 5,847+/-2,827 mm3 (P < 0.05) after nasal CPAP application.In contrast to the traditional view that relaxation of the tongue causes airway obstruction, this study suggests that airway closure occurs at the level of the soft palate. Application of nasal CPAP can counteract an anesthesia-induced pharyngeal narrowing by functioning as a pneumatic splint. This is supported by the observed reduction in anteroposterior diameter at the level of the soft palate during propofol anesthesia and the subsequent increase in this measurement during nasal CPAP application.