The role of the expiratory phase in obstructive sleep apnoea

Citation
O. Resta et al., The role of the expiratory phase in obstructive sleep apnoea, RESP MED, 93(3), 1999, pp. 190-195
Citations number
18
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
RESPIRATORY MEDICINE
ISSN journal
09546111 → ACNP
Volume
93
Issue
3
Year of publication
1999
Pages
190 - 195
Database
ISI
SICI code
0954-6111(199903)93:3<190:TROTEP>2.0.ZU;2-Z
Abstract
The role of the expiratory phase in obstructive sleep apnoea (OSA) is not w ell known, The aim of our study tvas to verify the contribution of expirato ry narrowing to apnoea in a group of OSA patients by evaluating the effects of short-term treatment with continuous positive airway pressure (CPAP). i ntermittent positive pressure ventilation (IPPV) and bi-level positive airw ay pressure (BIPAP). We studied a selected group of 10 OSA patients whose therapeutic pressure l evel of CPAP was at least 10 cm H2O During CPAP therapy the mean apnoea/hyp opnoea index (AHI) and oxyhaemoglobin desaturation index (ODI) decreased fr om 64.8 to 6.3(P<0.001) and from 58.5 to 6.1 (P<0.001), respectively and me an nadir SAO(2) increased from 62.0 to 91.6 (P<0.001). None of the patients reached optimal setting (elimination of snoring, reduc tion of apnoeas and non-apnoeic desaturation events at least to 15 or less per hour of sleep and maintenance of oxygen saturation approximately 90%) d uring IPPV and two patients did not tolerate final IPAP pressure levels. Wh en a critical level of EPAP (BIPAP) was applied in the same night to these patients, optimal setting was reached in all subjects. During BIPAP, mean A HI decreased from 64.8 to 7.4(P<0.001): ODI decreased from 58.5 to 7.6(P<0. 001) and nadir SAO(2) increased from 62.0 to 91.6 (P<0.001). Our study confirms the essential role of a critical level of EPAP in succes sful ventilatory treatment in OSA, thereby indicating, in agreement with fe w previous studies, the critical role of end of expiratory occlusion in OSA pathogenesis.