Anatomic abnormalities of the pharynx are thought to play a role in the pathogenesis of obstructive sleep apnea (OSA), but their contribution has never been conclusively proven. The present study tested this anatomic hypothesis by comparing the mechanics of the paralyzed pharynx in OSA patients and in normal subjects. According to evaluation of sleep-disordered breathing (SDB) by nocturnal oximetry, subjects were divided into three groups: normal group (n = 17), SDB-1 (n = 18), and SDB-2 (n = 22). The static pressure-area relationship of the passive pharynx was quantified under general anesthesia with complete paralysis. Age and body mass index were matched among the three groups. The site of the primary closure was the velopharynx in 49 subjects and the oropharynx in only 8 subjects. Distribution of the location of the primary closure did not differ among the groups. Closing pressure (PC) of the velopharynx for SDB-1 and SDB-2 groups (0.90 +/- 1.34 and 2.78 +/- 2.78 cmH2O, respectively) was significantly higher than that for the normal group (-3.77 +/- 3.44 cmH2O; P < 0.01). Maximal velopharyngeal area for the normal group (2.10 +/- 0.85 cm2) was significantly greater than for SDB-1 and SDB-2 groups (1.15 +/- 0.46 and 1.06 +/- 0.75 cm2, respectively). The shape of the pressure-area curve for the velopharynx differed between normal subjects and patients with SDB, being steeper in slope near Pc in patients with SDB. Multivariate analysis of mechanical parameters and oxygen desaturation index (ODI) revealed that velopharyngeal Pc was the only variable highly correlated with ODI. Velopharyngeal Pc was associated with oropharyngeal Pc, suggesting mechanical interdependence of these segments. We conclude that the passive pharynx is more narrow and collapsible in sleep-apneic patients than in matched controls and that velopharyngeal Pc is the principal correlate of the frequency of nocturnal desaturations.

The velopharynx is the most common site of obstruction in patients with obstructive sleep apnea (OSA). Advancement of the mandible effectively reverses the pharyngeal obstruction. Accordingly, we hypothesized that mandibular advancement increases cross-sectional area of several segments of the upper airway, including the velopharynx and the oropharynx. We examined the pressure-area properties of the pharyngeal airway in 13 patients with OSA. Under general anesthesia and total muscle paralysis, the pharynx was visualized with an endoscope connected to a video-recording system. During an experimentally induced apnea, we manipulated the nasal pressure from 20 cmH2O to the point of total closure at the velopharynx. The procedure was repeated after maximal forward displacement of the mandible. Measurements of the cross-sectional area at different levels of nasal pressure allowed construction of a static pressure-area relationship of the "passive pharynx," where active neuromuscular factors are suppressed. In 12 of 13 patients with OSA, advancement of the mandible stabilized the airway by reducing the closing pressure and increasing the area at any airway pressure. Thus the maneuver shifted the static pressure-area curve of the velopharynx and the oropharynx upward in these patients. We conclude that anterior movement of the mandible widens the retropalatal airway as well as that at the base of the tongue in the passive pharynx of OSA patients.

Mandibular advancement did not improve the retropalatal airway in obese persons.

Severe postoperative hypoxaemia during sleep may increase the risk of postoperative cardiovascular complications. We hypothesized that the severity of hypoxic episodes after surgery are related to the presence of preoperative sleep-disordered breathing (SDB). We tested this hypothesis in a multicentre study designed to elucidate the major risk factors for development of postoperative nocturnal desaturations. We performed overnight oximetry before operation and for one night between the second and fourth day after operation in 80 patients undergoing major surgery. We calculated oximetry variables such as oxygen desaturation index (ODI), defined as the number of oxygen desaturations exceeding 4% below baseline, percentage time spent at SpO2 < 90% (CT90, %) and lowest SpO2 value. After operation, although the change in ODI was not significant (P = 0.34), deterioration in CT90 and lowest SpO2 values were significant (P = 0.036 and P = 0.007, respectively). Multivariate analysis of possible risk factors for postoperative desaturations revealed that preoperative hypoxaemia and apnoea witnessed by others were highly correlated with postoperative hypoxaemia.

No abstract