We have observed patients who clinically have the obstructive sleep apnea syndrome but have no apneas, instead having recurrent nocturnal hypoventilation. There is disagreement about the definition and significance of such sleep-related hypopneas. We have thus analyzed breathing patterns, oxygenation and sleep records of 50 consecutive patients referred with the clinical features of the sleep apnea syndrome and found to have abnormal breathing during sleep to determine: (1) the best definition of hypopnea, and (2) how frequently patients have the clinical features of the sleep apnea syndrome without recurrent apneas. Hypopnea definitions based on decreases in thoracoabdominal movement yielded hypopnea frequencies that were significantly closer to desaturation and arousal frequencies than hypopnea definitions based on flow reduction. The best hypopnea definition was that of a 50% reduction in thoracoabdominal movement lasting for 10 s. This was validated in 33 normal subjects, all of whom had fewer than 11 hypopneas/h, and fewer than 14 apneas plus hypopneas/h of sleep. Thirty-two of the 50 patients had 10 or more apneas/h, the remaining 18 having 9 to 98 hypopneas/h such that all patients had more than 16 apneas plus hypopneas/h. Patients with recurrent hypopneas were clinically indistinguishable from and had a similar frequency of 4% desaturations (zero to 104/h) and arousals (7 to 98/h) to the patients with frequent apneas. This study confirms that hypopneas are clinically important and that the "sleep apnea syndrome" may occur in the absence of recurrent apneas.

Waiting times for hospital-based monitoring of the obstructive sleep apnoea/hypopnoea syndrome (OSAHS) are rising. This study tested whether Embletta, a new portable device, may accurately diagnose OSAHS at home.A synchronous comparison to polysomnography was performed in 40 patients and a comparison of home Embletta studies with in-laboratory polysomnography was performed in 61 patients.In the synchronous study, the mean difference (polysomnography–Embletta) in apnoeas+hypopnoeas (A+H)·h−1in bed was 2·h−1. In comparison to the apnoea/hypopnoea index (AHI)·h−1slept, the Embletta (A+H)·h−1in bed differed by 8·h−1. These data were used to construct diagnostic categories in symptomatic patients from their Embletta results: “OSAHS” (≥20 (A+H)·h−1in bed), “possible OSAHS” (10–20 (A+H)·h−1in bed) or “not OSAHS” (<10 (A+H)·h−1in bed). In the home study, the mean difference in (A+H)·h−1in bed was 3·h−1. In comparison to the polysomnographic AHI·h−1slept, the Embletta (A+H)·h−1in bed differed by 6±14·h−1. Using the above classification, all nine patients categorised as not OSAHS had AHI <15·h−1slept on polysomnography and all 23 with OSAHS on Embletta had an AHI ≥15 on polysomnography, but 18 patients fell into the possible OSAHS category potentially requiring further investigation and 11 home studies failed.Most patients were satisfactorily classified by home Embletta studies but 29 out of 61 required further investigation. The study suggested a 42% saving in diagnostic costs over polysomnography if this approach were adopted.

Most patients with sleep apnoea/hypopnoea syndrome (SAHS) are middle-aged men. As there are conflicting data on the effects of age and gender on upper airway calibre, we tested the hypothesis that increasing age and the male sex predispose to upper airway narrowing in normal subjects.We measured upper airway calibre using acoustic reflection in 60 men and 54 women (median 35, range 16-74 yrs) both seated and supine.All upper airway dimensions, except oropharyngeal junction (OPJ), decreased with increasing age in both men and women (r>-0.24, p≤0.05) while supine (r 2 >0.06). Men had greater changes in airway area at OPJ on lying down (mean (SEM) 0.5 (0.1), 0.2 (0.1) cm 2 ; p<0.02). Men had greater body mass indices (mean (SD) 26 (4), 24 (4) kg·m -2 ; p=0.04), and larger neck circumferences (mean (SD) 38 (3), 33 (2) cm; p<0.0001) than women. For any body mass index, neck circumference was larger in men than women (p<0.001).This study shows that upper airway size decreases with increasing age in both men and women, and that men have greater upper airway collapsibility on lying down at oropharyngeal junction than women. Eur Respir J 1997; 10: 2087-2090 The effects of age and gender on upper airway calibre are unclear. Clarification of their influences is important because the clinical condition associated with upper airway narrowing, the sleep apnoea/hypopnoea syndrome (SAHS), is predominantly a condition of middle-aged men [1]. BROOKS and STROHL [2] reported men to have larger upper airway calibre than women when seated and awake. Studies performed in the sitting position have indicated that upper airways resistance increases, and pharyngeal area decreases [3] with age in men but not in women. In contrast, computed tomography (CT) scan studies in supine men have shown no age-related increase in upper airway collapsibility in men [4]. In order to clarify this, we tested the hypothesis that increasing age and the male sex predispose to upper airway narrowing in the normal population. Methods SubjectsWe aimed to select a cross section of the local population and therefore recruited 60 male and 54 female subjects from the hospital workforce using an advertisement that did not refer to sleep. Their height, weight and neck circumference at the cricothyroid membrane were measured (table 1). Subjects were asked whether they snored and in which position, and whether they suffered from uncontrollable daytime sleepiness. Responses were noted but no one was excluded from the analysis as this was a population-based study. However, subjects with gross retrognathia were assessed clinically and excluded from the analysis. The study was approved by the local Ethics Advisory Committee.

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A B S T R A C T To determine the characteristics of and mechanisms causing the bradycardia during sleep apnea (SA), both patients with SA and normals were studied. Evaluation of six consecutive SA patients demonstrated that bradycardia occurred during 95% of all apneas (central, obstructive, and mixed) and became marked with increased apnea length (P < 0.01) and increased oxyhemoglobin desaturation (P < 0.01). Heart rate slowed 9.5 beats per minute (bpm) during apneas of 10-19 s in duration, 11.4 bpm during 20-39-s apneas, and 16.6 bpm during 40-59-s apneas. Sleep stage had no effect unexplained by apnea length or degree of desaturation.Oxygen administration to four SA patients completely prevented the bradycardia although apneas lengthened (P < 0.05) in three. Sleeping normal subjects did not develop bradycardia during hypoxic hyperpnea but, instead, HR increased with hypoxia in all sleep stages, although the increase in HR was not as great as that which occurred while awake.Breath holding in awake normals did not result in bradycardia during hyperoxia (SaO2 = 99%), but was consistently (P < 0.01) associated with heart rate slowing during room air breath-holds (-6 bpm) at SaO2 = 93%, with more striking slowing (-20 bpm) during hypoxic breath-holds (P < 0.01) at SaO2 = 78%. Breath holding during hyperoxic hypercapnia had no significant effect on rate. Breath holding in awake SA subjects demonstrated similar findings. We conclude that the bradycardia of SA is a consistent feature of apnea and results from the combined effect of cessation of breathing plus hypoxemia.