Prevalence and mechanisms of diurnal hypercapnia in a sample of morbidly obese subjects with obstructive sleep apnoea

Citation
O. Resta et al., Prevalence and mechanisms of diurnal hypercapnia in a sample of morbidly obese subjects with obstructive sleep apnoea, RESP MED, 94(3), 2000, pp. 240-246
Citations number
24
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
RESPIRATORY MEDICINE
ISSN journal
09546111 → ACNP
Volume
94
Issue
3
Year of publication
2000
Pages
240 - 246
Database
ISI
SICI code
0954-6111(200003)94:3<240:PAMODH>2.0.ZU;2-M
Abstract
It is well known that obstructive sleep apnoea is especially frequent in th e morbidly obese. In these subjects diurnal chronic hypercapnia, whose mech anism is still debated, may be present. Our study was performed to evaluate the prevalence and the mechanism of diu rnal hypercapnia in the morbidly obese affected by obstructive sleep apnoea . From a population referred to our centre because of suspicion of sleep re lated breathing disorders, we selected 285 subjects without cardiopulmonary , neuromuscular or endocrinological diseases: 89 (36 M and 53 F, aged 46+/- 13 years) had body mass index (BMI)greater than or equal to 40 kg m(-2) (MO group: morbidly obese subjects) and 196 (99 M and 97 F, aged 48+/-16 years ) had BMI < 40 kg m(-2) (NMO group: non-morbidly obese subjects). Then the MO group was divided into three subgroups: normocapnic subjects without obs tructive sleep apnoea, normocapnic subjects with obstructive sleep apnoea, hypercapnic subjects with obstructive sleep apnoea; while we found no hyper capnic subject without obstructive sleep apnoea. All subjects underwent anthropometric evaluations and bioelectrical impedan ce analyses, respiratory function tests and arterial blood gas analysis, a modified version of the Sleep and Healthy Questionnaire and a full night po lysomnography. Our results showed that hypercapnia (PaCO2 greater than or equal to 45 mmHg ) associated with obstructive sleep apnoea [respiratory disturbance index ( RDT) greater than or equal to 10 h(-1)] was found in 27% of the morbidly ob ese subjects, but only in 11% of the non-morbidly obese ones (P<0.01) The comparison among the three subgroups, in which we divided the morbidly obese subjects, shows that those with hypercapnia and obstructive sleep apn oea had significantly more important ventilatory restrictive defects [force d vital capacity (FVC)% of pred 73.27+/-14.81 vs. 82.37+/-16.93 vs. 87.25+/ -18.14 respectively; total lung capacity (TLC)% of pred 63.83+/-16.35 vs. 7 9.11+/-14.15 vs. 87.01+/-10.5], a significantly higher respiratory disturba nce index (RDI 46.34+/-26.90 vs. 31.79+/-22.47 vs. 4.98+/-3.29) a longer to tal sleep time with oxyhaemoglobin saturation < 90% [total sleeptime (TST)( SaO2, <90%) 63.40+/-33.86 vs. 25.95+/-29.34 vs. 8.22+/-22.12] and a lower r apid eye movement (REM) stage (9.5+/-1.2 vs. 14.0+/-0.9 vs. 17.05+/-1.2) th an normocapnic subjects with obstructive sleep apnoea or subjects without o bstructive sleep apnoea. The best model to predict PaCO2 resulted from a combination of TSTSaO2<90% (r(2) =0.22, P<0.001), forced expiratory volume in 1 sec (FEV1)% of pred (r (2) = 0.09. P <0.01), FVC % of pred (r(2) =0.075, P <0.01). In conclusion o ur study suggests that diurnal hypercapnia is frequently associated with ob structive sleep apnoea in the morbidly obese without chronic obstructive pu lmonary disorder (COPD) and that ventilatory restriction and sleep related respiratory disturbances correlate to diurnal hypercapnia.