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
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.