Obesity hypoventilation syndrome as a spectrum of respiratory disturbancesduring sleep

Citation
Ki. Berger et al., Obesity hypoventilation syndrome as a spectrum of respiratory disturbancesduring sleep, CHEST, 120(4), 2001, pp. 1231-1238
Citations number
22
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CHEST
ISSN journal
00123692 → ACNP
Volume
120
Issue
4
Year of publication
2001
Pages
1231 - 1238
Database
ISI
SICI code
0012-3692(200110)120:4<1231:OHSAAS>2.0.ZU;2-4
Abstract
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.