INDEXES FROM FLOW-VOLUME CURVES IN RELATION TO CEPHALOMETRIC, ENT-O-2AND SLEEP-O-2 SATURATION VARIABLES IN SNORERS WITH AND WITHOUT OBSTRUCTIVE SLEEP-APNEA
Jm. Bogaard et al., INDEXES FROM FLOW-VOLUME CURVES IN RELATION TO CEPHALOMETRIC, ENT-O-2AND SLEEP-O-2 SATURATION VARIABLES IN SNORERS WITH AND WITHOUT OBSTRUCTIVE SLEEP-APNEA, The European respiratory journal, 8(5), 1995, pp. 801-806
In a group of 37 heavy snorers with obstructive sleep apnoea (OSA, Gro
up 1) and a group of 23 heavy snorers without OSA (Group 2) cephalomet
ric indices, ENT indices related to upper airway collapsibility, and n
octurnal O-2 desaturation indices were related to variables from maxim
al expiratory and inspiratory flow-volume (MEFV and MIFV) curves. The
cephalometric indices used were the length and diameter of the soft pa
late (spl and spd), the shortest distance between the mandibular plane
and the hyoid bone (mph) and the posterior airway space (pas). Collap
sibility of the upper airways was observed at the level of the tongue
base and soft palate by fibroscopy during a Muller manoeuvre (mtb and
msp) and ranked on a five point scale, Sleep indices measured were the
mean number of oxygen desaturations of more than 3% per hour preceede
d by an apnoea or hypopnoea of more than 10 s (desaturation index), ma
ximal sleep oxygen desaturation, baseline arterial oxygen saturation (
Sa,O-2) and, in the OSA group, percentage of deep time with Si,O-2, <9
0%, The variables obtained from the flow-volume curves were the forced
vital capacity (FVC), forced expiratory and inspiratory volume in 1 s
(FEV1 and FIV1), peak expiratory and peak inspiratory flows (PEF and
PIF), and maximal flow after expiring 50% of the FVC (MEF50), The mean
of the flow-volume variables, influenced by upper airway aperture (PE
F, FIV1) was significantly greater than predicted. A significant corre
lation between flow-volume variables and the other indices was found o
nly for FIV1 (% pred), PEF (% pred) and for PIP with the maximal O-2 d
esaturation (r=-0.60, r=0.46, and r=-0.48, respectively) in the OSA gr
oup only. We hypothesize that compensatory mechanisms, which increase
the upper ah-way aperture during wakefulness, account for the raised P
EF, and FIV1. The decrease of PIF, PEF and FIV1, variables related to
upper airway aperture, with maximal O-2 desaturation can be explained
by the mechanisms relating sleep O-2 desaturation, chemical control of
tonic upper airway muscle activity, and upper airway aperture in OSA.