Objective: To identify the spectrum of respiratory disturbances during slee
p in patients with obesity hypoventilation syndrome (OHS) and to examine th
e response of hypercapnia to treatment of the specific ventilatory sleep di
sturbances.
Designs and methods: Twenty-three patients with chronic awake hypercapnia (
mean [ SD] PaCO2, 55 +/- 6 mm Hg) and a respiratory sleep disorder were ret
rospectively identified. Nocturnal polysomnography testing was performed, a
nd flow limitation (FL) was identified from the inspiratory, flow-time cont
our. Obstructive hypoventilation was inferred from sustained FL coupled wit
h O-2 desaturation that was corrected with treatment of the upper airway ob
struction. Central hypoventilation was inferred from sustained O-2 desatura
tion that persisted after the correction of the upper airway obstruction. T
reatment was initiated, and follow-up awake PaCO2 measurements were obtaine
d (follow-up range, 4 days to 7 years).
Results: A variable number of obstructive sleep apneas/hypopneas (ie, obstr
uctive sleep apnea-hypopnea syndrome [OSAHS]) were noted (range, 9 to 167 e
vents per hour of sleep). Of 23 patients, 11 demonstrated upper airway obst
ruction alone (apnea-hypopnea/FL) and 12 demonstrated central sleep hypoven
tilation syndrome (SHVS) in addition to a variable number of OSAHS. Treatme
nt aimed at correcting the specific ventilatory abnormalities resulted in c
orrection of the chronic hypercapnia in all compliant patients (compliant p
atients: pretreatment, 57 +/- 6 mm Hg vs post-treatment, 41 +/- 4 mm Hg [p
< 0.001]; noncompliant patients: pretreatment, 52 +/- 6 inn Hg vs post-trea
tment, 51 +/- 3 mm Hg; [difference not significant]).
Conclusions: This study demonstrates that OHS encompasses a variety of dist
inct pathophysiologic disturbances that cannot be distinguished clinically
at presentation. Sustained obstructive hypoventilation due to partial upper
airway obstruction was demonstrated as an additional mechanism for OHS tha
t is not easily, classified as SHVS or OSAHS.