The aim of the present study was to assess whether nasal continuous positive airway pressure (nCPAP) treatment, applied for only a few hours at the beginning of the night, has any residual effect on sleep and breathing during the ensuing hours of unassisted sleep in patients with obstructive sleep apnoea syndrome (OSAS).In 27 patients with newly-diagnosed OSAS, effective nCPAP was applied during the first part of the night and then withdrawn. Polysomnographic parameters after nCPAP withdrawal were compared with those of the corresponding part of the diagnostic polysomnography performed a few days or weeks before and with those of the first part of night on nCPAP.After 255±63 (mean±SD) min of sleep with normalization of sleep and breathing parameters under nCPAP, there was partial improvement of OSAS severity during the remaining 124±56 min of nocturnal sleep without treatment; mean oxygen saturation, desaturation index (equivalent to the apnoea/hypopnoea index) and movement arousal index all improved significantly with respect to the diagnostic night (p=0.001). This improvement was not accounted for by a change in sleep architecture.We conclude that there is an improvement in severity of obstructive sleep apnoea syndrome after only 4 h of nasal continuous positive airway pressure. This carryover effect could explain why a number of patients with obstructive sleep apnoea syndrome apply nasal continuous positive airway pressure for only part of the night or not every night. Eur Respir J 1997; 10: 973-976.

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We measured in healthy volunteers airway resistance (R(aw)), resistance of the respiratory system (Rrs), and supralaryngeal resistance (Rsl) in the following head positions: neutral, extended, and partially and fully flexed. Sagittal magnetic resonance images of the upper airways were recorded in neutral and flexed head positions. We observed significant increases in Raw (P less than 0.01), Rrs (P less than 0.001), and Rsl (P less than 0.001) in the flexed position, with respect to the neutral one, and corresponding decreases of specific airway and specific respiratory conductances. Resistances decreased (although not significantly) when the subjects' heads were extended. A decrease in both diameter and surface area of the hypopharyngeal airways (as shown by magnetic resonance images) with total head flexion was accompanied by significant increases in all measured resistances. Changes in the caliber of hypopharynx appear to be responsible for the increase in resistance during head flexion.

We have previously produced evidence that, in patients with obstructive lung disease, compliance of extrathoracic airways is responsible for lack of mouth-to-alveolar pressure equilibration during respiratory efforts against a closed airway. The flow interruption method for measuring respiratory resistance (Rint) is potentially faced with the same problems. We reassessed the merits of the interruption technique by rendering the extrathoracic airways more rigid and by using a rapid shutter. We measured airway resistance (Raw) with whole body plethysmography during panting (at 2 Hz) and Rint during quiet breathing. Rint and Raw were expressed as specific airway (sGaw) and interruptive conductance (sGint), respectively. In nine healthy subjects (cheeks supported), sGint (0.140 +/- 0.050 s-1.cmH2O-1) was lower (P less than 0.02) than sGaw (0.182 +/- 0.043 s-1.cmH2O-1). By contrast, in 12 patients with severe obstructive lung disease (forced expiratory volume in 1 s/vital capacity = 41.0 +/- 19.8%), sGint (0.058 +/- 0.012 s-1.cmH2O-1) was higher (P less than 0.05) than sGaw (0.047 +/- 0.007 s-1.cmH2O-1), when the cheeks were supported. When the mouth floor was also supported, average values of sGaw (0.048 +/- 0.008 s-1.cmH2O-1) and sGint (0.049 +/- 0.014 s-1.cmH2O-1) became similar. In conclusion, we confirm previous findings in healthy subjects of higher values of Rint, with respect to Raw, probably because of differences in glottis opening between quiet breathing and panting. In airflow obstruction, supporting both the cheeks and the mouth floor decreased sGint, which became similar to sGaw.

Expiratory pressure-volume curves and maximal expiratory flow-volume curves were obtained in 74 healthy subjects (49 males 25 females) aged between 20 and 64. Maximal expiratory flowstatic recoil (MEFSR) curves were then constructed. Aging was associated with loss of lung recoil and reduction in maximal expiratory flow measured between 80 and 50% total lung capacity (TLC), in both males and females, with the slope of the MEFSR curve becoming steeper. In subjects less than 40 yr old the conductance of the upstream segment increased from 80 to 50% TLC, whereas in older subjects it decreased. We also studied the effects of alveolar gas compression artifacts on MEFSR curves in 12 additional subjects and 10 patients with chronic obstructive lung disease; consistent changes were found, but the subsequent shift of the MEFSR curve toward the left was only mild. These changes are interpreted as reflecting the net effects of an increase in the unstressed dimensions of the airways together with a decrease in intraparenchymal airways diameter, probably due to loss of parenchymal airways diameter, probably due to loss of parenchymal support. It was also concluded that the analysis of the MEFSR curve did not allow a quantitative estimate of the chantes in airways compressibility with aging.