Treatment Effects on Carbon Dioxide Retention in Patients With Obstructive Sleep Apnea-Hypopnea Syndrome
This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO2 retention. We recruited 10 body mass index-matched, apnea-hypopnea index-matched, age-matched, and lung function-matched OSAHS patients, according to their a...
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Published in | Chest Vol. 119; no. 6; pp. 1814 - 1819 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Northbrook, IL
Elsevier Inc
01.06.2001
American College of Chest Physicians |
Subjects | |
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Abstract | This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO2 retention.
We recruited 10 body mass index-matched, apnea-hypopnea index-matched, age-matched, and lung function-matched OSAHS patients, according to their awake Paco2. Five patients were hypercapnic (Paco2, ≥ 45 mm Hg), and five patients were eucapnic. Hypoxic responses (the ratio of the change in minute ventilation [Δ V˙e] to the change in arterial oxygen saturation[ΔSao2] and the ratio of the change in mouth occlusion pressure over the first 100 ms of inspiration against an occluded airway [ΔP0.1] to Δ Sao2) and hypercapnic responses (Δ V˙e/ΔPco2 ratio andΔP0.1/ΔPco2 ratio) were testedduring wakefulness before treatment in all 10 patients, and before and during treatment (at 2, 4, and 6 weeks) with pressure support in the hypercapnic group.
Hypercapnic patients had lower mean (± SD)Δ V˙e/Δ Sao2 ratio than eucapnic patients (−0.17 ± 0.04 vs −0.34 ± 0.04 L /min/% Sao2, respectively), lower meanΔP0.1/Δ Sao2 ratio(−0.04 ± 0.02 vs −0.14 ± 0.03 cm H2O/% Sao2, respectively), and lower ΔP0.1/ΔPco2 ratio(0.23 ± 0.1 vs 0.49 ± 0.1 cm H2O/mm Hg, respectively)[p < 0.05]. After receiving noninvasive ventilation treatment, the hypercapnic and hypoxic responses of the hypercapnic patients increased. At 4 to 6 weeks, values for both responses had increased to within the normal range and Paco2 had fallen to< 45 mm Hg, while weight was unchanged.
Depressed chemoresponsiveness plays a role that is independent of obesity in the development of CO2 retention in some OSAHS patients, and it may be a response to sleep-disordered breathing. |
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AbstractList | Objectives: This study was designed to examine
respiratory control in patients with obstructive sleep apnea-hypopnea
syndrome (OSAHS), with or without CO 2 retention.
Methods: We recruited 10 body mass index-matched,
apnea-hypopnea index-matched, age-matched, and lung function-matched
OSAHS patients, according to their awake Pa co 2 .
Five patients were hypercapnic (Pa co 2 , ⥠45
mm Hg), and five patients were eucapnic. Hypoxic responses (the ratio
of the change in minute ventilation [ÎVÌ e ] to the
change in arterial oxygen saturation[Î
Sa o 2 ] and the ratio of the change in
mouth occlusion pressure over the first 100 ms of inspiration against
an occluded airway [ÎP 0.1 ] toÎ
Sa o 2 ) and hypercapnic responses
(ÎVÌ e /ÎP co 2 ratio andÎ
P 0.1 /ÎP co 2 ratio) were tested
during wakefulness before treatment in all 10 patients, and before and
during treatment (at 2, 4, and 6 weeks) with pressure support in the
hypercapnic group.
Results: Hypercapnic
patients had lower mean (± SD)Î
VÌ e /ÎSa o 2 ratio than
eucapnic patients (â0.17 ± 0.04 vs â0.34 ± 0.04
L /min/%Sa o 2 , respectively), lower meanÎ
P 0.1 /ÎSa o 2 ratio
(â0.04 ± 0.02 vs â0.14 ± 0.03 cm
H 2 O/%Sa o 2 , respectively), and
lower ÎP 0.1 /ÎP co 2 ratio
(0.23 ± 0.1 vs 0.49 ± 0.1 cm H 2 O/mm Hg, respectively)[
p < 0.05]. After receiving noninvasive ventilation treatment, the
hypercapnic and hypoxic responses of the hypercapnic patients
increased. At 4 to 6 weeks, values for both responses had increased to
within the normal range and Pa co 2 had fallen to< 45 mm Hg, while weight was unchanged.
Conclusions:
Depressed chemoresponsiveness plays a role that is independent of
obesity in the development of CO 2 retention in some OSAHS
patients, and it may be a response to sleep-disordered
breathing. OBJECTIVESThis study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO(2) retention.METHODSWe recruited 10 body mass index-matched, apnea-hypopnea index-matched, age-matched, and lung function-matched OSAHS patients, according to their awake PaCO(2). Five patients were hypercapnic (PaCO(2), > or = 45 mm Hg), and five patients were eucapnic. Hypoxic responses (the ratio of the change in minute ventilation [DeltaV(E)] to the change in arterial oxygen saturation [DeltaSaO(2)] and the ratio of the change in mouth occlusion pressure over the first 100 ms of inspiration against an occluded airway [DeltaP(0.1)] to DeltaSaO(2)) and hypercapnic responses (DeltaV(E)/DeltaPCO(2) ratio and DeltaP(0.1)/DeltaPCO(2) ratio) were tested during wakefulness before treatment in all 10 patients, and before and during treatment (at 2, 4, and 6 weeks) with pressure support in the hypercapnic group.RESULTSHypercapnic patients had lower mean (+/- SD) DeltaV(E)/DeltaSaO(2) ratio than eucapnic patients (-0.17 +/- 0.04 vs -0.34 +/- 0.04 L /min/%SaO(2), respectively), lower mean DeltaP(0.1)/DeltaSaO(2) ratio (-0.04 +/- 0.02 vs -0.14 +/- 0.03 cm H(2)O/%SaO(2), respectively), and lower DeltaP(0.1)/DeltaPCO(2) ratio (0.23 +/- 0.1 vs 0.49 +/- 0.1 cm H(2)O/mm Hg, respectively) [p < 0.05]. After receiving noninvasive ventilation treatment, the hypercapnic and hypoxic responses of the hypercapnic patients increased. At 4 to 6 weeks, values for both responses had increased to within the normal range and PaCO(2) had fallen to < 45 mm Hg, while weight was unchanged.CONCLUSIONSDepressed chemoresponsiveness plays a role that is independent of obesity in the development of CO(2) retention in some OSAHS patients, and it may be a response to sleep-disordered breathing. This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO(2) retention. We recruited 10 body mass index-matched, apnea-hypopnea index-matched, age-matched, and lung function-matched OSAHS patients, according to their awake PaCO(2). Five patients were hypercapnic (PaCO(2), > or = 45 mm Hg), and five patients were eucapnic. Hypoxic responses (the ratio of the change in minute ventilation [DeltaV(E)] to the change in arterial oxygen saturation [DeltaSaO(2)] and the ratio of the change in mouth occlusion pressure over the first 100 ms of inspiration against an occluded airway [DeltaP(0.1)] to DeltaSaO(2)) and hypercapnic responses (DeltaV(E)/DeltaPCO(2) ratio and DeltaP(0.1)/DeltaPCO(2) ratio) were tested during wakefulness before treatment in all 10 patients, and before and during treatment (at 2, 4, and 6 weeks) with pressure support in the hypercapnic group. Hypercapnic patients had lower mean (+/- SD) DeltaV(E)/DeltaSaO(2) ratio than eucapnic patients (-0.17 +/- 0.04 vs -0.34 +/- 0.04 L /min/%SaO(2), respectively), lower mean DeltaP(0.1)/DeltaSaO(2) ratio (-0.04 +/- 0.02 vs -0.14 +/- 0.03 cm H(2)O/%SaO(2), respectively), and lower DeltaP(0.1)/DeltaPCO(2) ratio (0.23 +/- 0.1 vs 0.49 +/- 0.1 cm H(2)O/mm Hg, respectively) [p < 0.05]. After receiving noninvasive ventilation treatment, the hypercapnic and hypoxic responses of the hypercapnic patients increased. At 4 to 6 weeks, values for both responses had increased to within the normal range and PaCO(2) had fallen to < 45 mm Hg, while weight was unchanged. Depressed chemoresponsiveness plays a role that is independent of obesity in the development of CO(2) retention in some OSAHS patients, and it may be a response to sleep-disordered breathing. OBJECTIVES: This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO(2) retention. METHODS: We recruited 10 body mass index-matched, apnea-hypopnea index-matched, age-matched, and lung function-matched OSAHS patients, according to their awake PaCO(2). Five patients were hypercapnic (PaCO(2), > or = 45 mm Hg), and five patients were eucapnic. Hypoxic responses (the ratio of the change in minute ventilation [DeltaV(E)] to the change in arterial oxygen saturation [DeltaSaO(2)] and the ratio of the change in mouth occlusion pressure over the first 100 ms of inspiration against an occluded airway [DeltaP(0.1)] to DeltaSaO(2)) and hypercapnic responses (DeltaV(E)/DeltaPCO(2) ratio and DeltaP(0.1)/DeltaPCO(2) ratio) were tested during wakefulness before treatment in all 10 patients, and before and during treatment (at 2, 4, and 6 weeks) with pressure support in the hypercapnic group. RESULTS: Hypercapnic patients had lower mean (+/- SD) DeltaV(E)/DeltaSaO(2) ratio than eucapnic patients (-0.17 +/- 0.04 vs -0.34 +/- 0.04 L /min/%SaO(2), respectively), lower mean DeltaP(0.1)/DeltaSaO(2) ratio (-0.04 +/- 0.02 vs -0.14 +/- 0.03 cm H(2)O/%SaO(2), respectively), and lower DeltaP(0.1)/DeltaPCO(2) ratio (0.23 +/- 0.1 vs 0.49 +/- 0.1 cm H(2)O/mm Hg, respectively) [p < 0.05]. After receiving noninvasive ventilation treatment, the hypercapnic and hypoxic responses of the hypercapnic patients increased. At 4 to 6 weeks, values for both responses had increased to within the normal range and PaCO(2) had fallen to < 45 mm Hg, while weight was unchanged. CONCLUSIONS: Depressed chemoresponsiveness plays a role that is independent of obesity in the development of CO(2) retention in some OSAHS patients, and it may be a response to sleep-disordered breathing. This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO2 retention. We recruited 10 body mass index-matched, apnea-hypopnea index-matched, age-matched, and lung function-matched OSAHS patients, according to their awake Paco2. Five patients were hypercapnic (Paco2, ≥ 45 mm Hg), and five patients were eucapnic. Hypoxic responses (the ratio of the change in minute ventilation [Δ V˙e] to the change in arterial oxygen saturation[ΔSao2] and the ratio of the change in mouth occlusion pressure over the first 100 ms of inspiration against an occluded airway [ΔP0.1] to Δ Sao2) and hypercapnic responses (Δ V˙e/ΔPco2 ratio andΔP0.1/ΔPco2 ratio) were testedduring wakefulness before treatment in all 10 patients, and before and during treatment (at 2, 4, and 6 weeks) with pressure support in the hypercapnic group. Hypercapnic patients had lower mean (± SD)Δ V˙e/Δ Sao2 ratio than eucapnic patients (−0.17 ± 0.04 vs −0.34 ± 0.04 L /min/% Sao2, respectively), lower meanΔP0.1/Δ Sao2 ratio(−0.04 ± 0.02 vs −0.14 ± 0.03 cm H2O/% Sao2, respectively), and lower ΔP0.1/ΔPco2 ratio(0.23 ± 0.1 vs 0.49 ± 0.1 cm H2O/mm Hg, respectively)[p < 0.05]. After receiving noninvasive ventilation treatment, the hypercapnic and hypoxic responses of the hypercapnic patients increased. At 4 to 6 weeks, values for both responses had increased to within the normal range and Paco2 had fallen to< 45 mm Hg, while weight was unchanged. Depressed chemoresponsiveness plays a role that is independent of obesity in the development of CO2 retention in some OSAHS patients, and it may be a response to sleep-disordered breathing. |
Author | He, Quanying Chen, Erzhang Ding, Dongjie Han, Fang Wei, Hailing Strohl, Kingman P. |
Author_xml | – sequence: 1 givenname: Fang surname: Han fullname: Han, Fang organization: Department of Medicine, Louis Stokes VA Medical Center, Case Western Reserve University, Cleveland, OH – sequence: 2 givenname: Erzhang surname: Chen fullname: Chen, Erzhang organization: Department of Medicine, People’s Hospital, Medical School of Beijing University, Beijing, China – sequence: 3 givenname: Hailing surname: Wei fullname: Wei, Hailing organization: Department of Medicine, People’s Hospital, Medical School of Beijing University, Beijing, China – sequence: 4 givenname: Quanying surname: He fullname: He, Quanying organization: Department of Medicine, People’s Hospital, Medical School of Beijing University, Beijing, China – sequence: 5 givenname: Dongjie surname: Ding fullname: Ding, Dongjie organization: Department of Medicine, People’s Hospital, Medical School of Beijing University, Beijing, China – sequence: 6 givenname: Kingman P. surname: Strohl fullname: Strohl, Kingman P. email: KPSTROHL@aol.com organization: Department of Medicine, Louis Stokes VA Medical Center, Case Western Reserve University, Cleveland, OH |
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Keywords | respiratory control SIT90 obstructive sleep apnea-hypopnea syndrome AHI CPAP MAHT V˙e ESS P0.1 NREM CO2 retention TST Sao2 OSAHS SL MSao2 REM BMI Human Hypercapnia Sleep apnea syndrome Oxygen Prognosis Treatment Respiratory disease Follow up study Carbon dioxide Hypoxia |
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References | Greenberg, Scharf (bib21) 1993; 148 Schaeffer, Hastings, Carey (bib14) 1963; 18 Orlowski, Herrell, Moodie (bib16) 1982; 10 Findley, Boykin, Fallon (bib18) 1988; 64 Leech, Onal, Aronson (bib25) 1991; 100 Leech, Onal, Baer (bib6) 1987; 92 Rapoport, Garay, Epstein (bib15) 1986; 89 Redline, Leitner, Arnold (bib20) 1997; 156 Clark, Sinclair, Welch (bib13) 1979; 46 Rechtschaffen, Kales (bib9) 1968 Strohl, Hensley, Saunders (bib27) 1981; 245 Guilleminault, Cummiskey (bib24) 1982; 126 Bleich, Berkman, Schwartz (bib12) 1964; 43 Lyons, Huang (bib26) 1968; 44 Read (bib10) 1967; 16 Jones, Wilhoit, Findley (bib7) 1985; 88 Strohl (bib17) 1996; 153 Lopata, Onal (bib19) 1982; 126 Rebuck, Campbell (bib11) 1974; 109 Verbraecken, De Backer, Willemen (bib23) 1995; 101 Zwillich, Sutton, Pierson (bib4) 1975; 59 Resta, Foschino-Barbaro, Bonfitto (bib1) 2000; 94 Chaouat, Weitzenblum, Krieger (bib2) 1996; 109 Lin (bib5) 1994; 7 Bradley, Rutherford, Lue (bib3) 1986; 134 Gozal, Torres, Menendez (bib22) 1996; 9 Black, Hyatt (bib8) 1971; 103 Chaouat (10.1378/chest.119.6.1814_bib2) 1996; 109 Strohl (10.1378/chest.119.6.1814_bib17) 1996; 153 Leech (10.1378/chest.119.6.1814_bib25) 1991; 100 Leech (10.1378/chest.119.6.1814_bib6) 1987; 92 Bleich (10.1378/chest.119.6.1814_bib12) 1964; 43 Verbraecken (10.1378/chest.119.6.1814_bib23) 1995; 101 Clark (10.1378/chest.119.6.1814_bib13) 1979; 46 Rapoport (10.1378/chest.119.6.1814_bib15) 1986; 89 Rechtschaffen (10.1378/chest.119.6.1814_bib9) 1968 Bradley (10.1378/chest.119.6.1814_bib3) 1986; 134 Jones (10.1378/chest.119.6.1814_bib7) 1985; 88 Redline (10.1378/chest.119.6.1814_bib20) 1997; 156 Lyons (10.1378/chest.119.6.1814_bib26) 1968; 44 Strohl (10.1378/chest.119.6.1814_bib27) 1981; 245 Lopata (10.1378/chest.119.6.1814_bib19) 1982; 126 Gozal (10.1378/chest.119.6.1814_bib22) 1996; 9 Greenberg (10.1378/chest.119.6.1814_bib21) 1993; 148 Resta (10.1378/chest.119.6.1814_bib1) 2000; 94 Zwillich (10.1378/chest.119.6.1814_bib4) 1975; 59 Orlowski (10.1378/chest.119.6.1814_bib16) 1982; 10 Black (10.1378/chest.119.6.1814_bib8) 1971; 103 Guilleminault (10.1378/chest.119.6.1814_bib24) 1982; 126 Rebuck (10.1378/chest.119.6.1814_bib11) 1974; 109 Read (10.1378/chest.119.6.1814_bib10) 1967; 16 Lin (10.1378/chest.119.6.1814_bib5) 1994; 7 Schaeffer (10.1378/chest.119.6.1814_bib14) 1963; 18 Findley (10.1378/chest.119.6.1814_bib18) 1988; 64 |
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Snippet | This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO2 retention.
We... Objectives: This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO 2... This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO(2) retention. We... OBJECTIVES: This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO(2)... OBJECTIVESThis study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO(2)... |
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SubjectTerms | Adult Biological and medical sciences Body mass index Carbon Dioxide - metabolism Chemoreceptor Cells - physiopathology CO2 retention Electromyography Eye movements Female Humans Hypoventilation Hypoxia Hypoxia - physiopathology Male Medical sciences Middle Aged Neuromuscular diseases Obesity Obesity - complications obstructive sleep apnea-hypopnea syndrome Oxygen saturation Patients Pneumology Positive-Pressure Respiration respiratory control Respiratory system : syndromes and miscellaneous diseases Retention Sleep - physiology Sleep apnea Sleep Apnea, Obstructive - physiopathology Sleep Apnea, Obstructive - therapy Sleep disorders |
Title | Treatment Effects on Carbon Dioxide Retention in Patients With Obstructive Sleep Apnea-Hypopnea Syndrome |
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