title: Effects of stabilizing or increasing respiratory motor outputs on obstructive sleep apnea.
abstract: To determine how the obstructive sleep apnea (OSA) patient's pathophysiological traits predict the success of the treatment aimed at stabilization or increase in respiratory motor outputs, we studied 26 newly diagnosed OSA patients [apnea-hypopnea index (AHI) 42 ± 5 events/h with 92% of apneas obstructive] who were treated with O2 supplementation, an isocapnic rebreathing system in which CO2 was added only during hyperpnea to prevent transient hypocapnia, and a continuous rebreathing system. We also measured each patient's controller gain below eupnea [change in minute volume/change in end-tidal Pco2 (ΔVe/ΔPetCO2)], CO2 reserve (eupnea-apnea threshold PetCO2), and plant gain (ΔPetCO2/ΔVe), as well as passive upper airway closing pressure (Pcrit). With isocapnic rebreathing, 14/26 reduced their AHI to 31 ± 6% of control (P < 0.01) (responder); 12/26 did not show significant change (nonresponder). The responders vs. nonresponders had a greater controller gain (6.5 ± 1.7 vs. 2.1 ± 0.2 l·min(-1)·mmHg(-1), P < 0.01) and a smaller CO2 reserve (1.9 ± 0.3 vs. 4.3 ± 0.4 mmHg, P < 0.01) with no differences in Pcrit (-0.1 ± 1.2 vs. 0.2 ± 0.9 cmH2O, P > 0.05). Hypercapnic rebreathing (+4.2 ± 1 mmHg PetCO2) reduced AHI to 15 ± 4% of control (P < 0.001) in 17/21 subjects with a wide range of CO2 reserve. Hyperoxia (SaO2 ∼95-98%) reduced AHI to 36 ± 11% of control in 7/19 OSA patients tested. We concluded that stabilizing central respiratory motor output via prevention of transient hypocapnia prevents most OSA in selected patients with a high chemosensitivity and a collapsible upper airway, whereas increasing respiratory motor output via moderate hypercapnia eliminates OSA in most patients with a wider range of chemosensitivity and CO2 reserve. Reducing chemosensitivity via hyperoxia had a limited and unpredictable effect on OSA.
authors.affiliation: James B. Skatrud Laboratory of Pulmonary and Sleep Medicine, William S. Middleton Memorial Veterans Affairs Hospital, Madison, WI 53705, USA. axie@wisc.edu
authors.forename: Ailiang
authors.initials: A
authors.lastname: Xie
authors.forename: Mihaela
authors.initials: M
authors.lastname: Teodorescu
authors.forename: David F
authors.initials: DF
authors.lastname: Pegelow
authors.forename: Mihai C
authors.initials: MC
authors.lastname: Teodorescu
authors.forename: Yuansheng
authors.initials: Y
authors.lastname: Gong
authors.forename: Jessica E
authors.initials: JE
authors.lastname: Fedie
authors.forename: Jerome A
authors.initials: JA
authors.lastname: Dempsey
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001143:Arousal; D015992:Body Mass Index; D001945:Breathing Exercises; D002245:Carbon Dioxide / Q000378:metabolism; D003627:Data Interpretation, Statistical; D005260:Female; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D018496:Hyperoxia / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D017286:Polysomnography; D011659:Pulmonary Gas Exchange; D015656:Respiratory Mechanics / Q000502:physiology; D020181:Sleep Apnea, Obstructive / Q000145:classification / Q000534:rehabilitation / Q000628:therapy*; D055815:Young Adult
chemical_list: D002245:Carbon Dioxide
keywords: hypercapnia; hyperoxia; isocapnia