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.
Nocturnal polysomnography, the standard diagnostic test for sleep apnea, is an expensive and limited resource. In order to help identify the urgency of need for treatment, we determined which clinical features were most useful for establishing an accurate estimate of the probability that a patient had sleep apnea. Of 263 physician-referred patients, 200 were eligible for the study and 180 (90%) completed it. All patients had their histories recorded with a standard questionnaire, and underwent anthropomorphic measurements and nocturnal polysomnography. Sleep apnea was defined as more than 10 episodes of apnea or hypopnea per hour of sleep. Multiple linear and logistic regression models predictive of sleep apnea were compared with physicians' subjective impressions and previously reported models. Likelihood ratios were calculated for several levels of a sleep apnea clinical score produced by one of the linear models. Predictors of sleep apnea in the final model (R2 = 0.34) included neck circumference, hypertension, habitual snoring, and bed partner reports of nocturnal gasping/choking respirations. This model was superior to physician impression, slightly inferior to more detailed linear and logistic models, and comparable to previously reported models. A sleep apnea clinical score of less than 5 had a likelihood ratio of 0.25 (95% CI: 0.15 to 0.42) and a corresponding posttest probability of 17%, while a score of greater than 15 had a likelihood ratio of 5.17 (95% CI: 2.54 to 10.51) and posttest probability of 81%. These likelihood ratios can simply and accurately determined the probability of whether a patient has sleep apnea.
Using prospectively established rules for interpreting the polysomnographic data, the mandibular titration study predicted mandibular repositioning appliance therapeutic outcome with significant accuracy, particularly with regard to accurately predicting therapeutic success. As well, among the participants predicted to be therapeutically successful with mandibular repositioning appliance therapy, the effective target protrusive position provided efficacious mandibular protrusion in the majority.
Based on previous studies, we hypothesized that the pharynx collapses at multiple sites in most patients with obstructive sleep apnea (OSA). The purpose of this study was to document, in a population of apneic subjects, the site(s) of narrowing and closing pressure of the hypotonic pharynx. We endoscopically examined the pharynx in 45 OSA patients during sleep while they received nasal continuous positive airway pressure (CPAP), which produces hypotonia of pharyngeal muscles. Intrapharyngeal images and pressures were obtained at the end of expiration during single-breath tests (SBT). The fractional narrowing (FN) of each pharyngeal segment (nasopharynx, oropharynx, and hypopharynx) was calculated as the relative change in area when nasal airway pressure was reduced from a pressure that held the pharynx fully distended to the pressure at which the airway closed. The frequency distribution of FN for the nasopharynx was skewed toward larger values, and the frequency was relatively evenly distributed for the oropharynx and hypopharynx. A site having FN greater than 0.75 was defined as a site of primary narrowing, and a site showing FN 0.25 to 0.75 was defined as a site of secondary narrowing. The nasopharynx was a site of primary narrowing in 80% of patients, and two or more sites of narrowing were commonly observed (82%). Four categories of combined narrowing were identified: (1) primary narrowing only at the nasopharynx (18%); (2) primary narrowing at the nasopharynx plus other sites of secondary narrowing (40%); (3) primary narrowing at the nasopharynx plus other sites of primary narrowing (22%); and (4) other patterns (20%).(ABSTRACT TRUNCATED AT 250 WORDS)
Obstructive sleep apnea (OSA) is traditionally diagnosed using overnight polysomnography. Decision rules may provide an alternative to polysomnography. A consecutive series of patients referred to a tertiary sleep center underwent prospective evaluation with the upper airway physical examination protocol, followed by determination of the respiratory disturbance index using a portable monitor. Seventy-five patients were evaluated with the upper airway physical examination protocol. Historic predictors included age, snoring, witnessed apneas, and hypertension. Physical examination-based predictors included body mass index, neck circumference, mandibular protrusion, thyro-rami distance, sterno-mental distance, sterno-mental displacement, thyro-mental displacement, cricomental space, pharyngeal grade, Sampsoon-Young classification, and over-bite. A decision rule was developed using three predictors: a cricomental space of 1.5 cm or less, a pharyngeal grade of more than II, and the presence of overbite. In patients with all three predictors (17%), the decision rule had a positive predictive value of 95% (95% confidence interval [CI], 75-100%) and a negative predictive value of 49% (95% CI, 35-63%). A cricomental space of more than 1.5 cm (27% of patients) excluded OSA (negative predictive value of 100%, 95% CI, 75-100%). Comparable performance was obtained in a validation sample of 50 patients referred for diagnostic testing. This decision rule provides a simple, reliable, and accurate method of identifying a subset patients with, and perhaps more importantly, without OSA.
To determine if there was a relationship between cardiac arrhythmias and sleep apnea, we studied the prevalence of arrhythmias in a consecutive series of patients referred to our clinic for assessment of this disorder. Two hundred of 263 physician-referred patients were eligible for the study and, of these, 173 (86.5%) had complete investigations. All patients underwent a full night of polysomnography and Holter monitoring. Sleep apnea was diagnosed if patients had more than 10 apneas and hypopneas per hour (AHI). In 76 patients (43.9%) sleep apnea was diagnosed (median AHI = 33). The prevalence of arrhythmias in patients with sleep apnea versus those without was, respectively: complex ventricular ectopy (including ventricular tachycardia), 1.3% (95% CI, 0.4 to 6.9) versus 4.1% (CI, 1.6 to 10.1); frequent ventricular premature beats (> 30/h), 2.6% (CI, 0.8 to 8.9) versus 6.2% (CI, 2.9 to 12.8); second-degree atrioventricular block, 1.3% (CI, 0.4 to 6.9) versus 4.1% (CI, 1.6 to 10.1); sinus arrest, 5.2% (CI, 2.2 to 12.6) versus 1.0% (CI, 0.2 to 5.6). None of these differences was statistically significant. We conclude that the prevalence of cardiac arrhythmias is low in patients without serious cardiac or respiratory comorbidity who are referred for assessment of sleep apnea. Furthermore, the presence or absence of arrhythmias in this group is unrelated to sleep apnea severity.
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