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Effects of Noninvasive Positive Pressure Ventilation on Gas Exchange and Sleep in COPD Patients

Samuel L. Krachman; A. J. Quaranta; Thomas J. Berger; Gerard J. Criner
Author and Funding Information

Affiliations: From the Sleep Disorders Center, Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia,  From the Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia,  From the Sleep Disorders Center, Temple University School of Medicine, Philadelphia

Affiliations: From the Sleep Disorders Center, Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia,  From the Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia,  From the Sleep Disorders Center, Temple University School of Medicine, Philadelphia

Affiliations: From the Sleep Disorders Center, Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia,  From the Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia,  From the Sleep Disorders Center, Temple University School of Medicine, Philadelphia


1997 by the American College of Chest Physicians


Chest. 1997;112(3):623-628. doi:10.1378/chest.112.3.623
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Abstract

Study objective: The role of nocturnal noninvasive positive pressure ventilation (NPPV) in the treatment of patients with hypercapnic COPD remains controversial. Beneficial effects reported after prolonged use have included an improvement in gas exchange. The purpose of this study was to examine the short-term effects of NPPV on gas exchange and sleep characteristics in patients with hypercapnic COPD and to determine if similar acute changes in gas exchange are associated with improved sleep quality.

Design: Prospective, randomized, controlled trial.

Setting: Sleep laboratory of a university hospital.

Patients: Six patients with severe but stable hypercapnic COPD (PaCO2=58±4 [SE] mm Hg). Mean age was 63±6 (SD) with an FEV1=0.58±0.09 L.

Interventions and measurements: Patients were studied in the sleep laboratory for a total of three nights. On nights 2 and 3, arterial catheters were placed prior to the study. Following an acquaintance night, patients were randomized to either a control-sham night on 5 cm H2O nasal continuous positive airway pressure (CPAP) or an NPPV night using a ventilatory support system (BiPAP; Respironics Inc; Murrysville, Pa) at previously determined optimal settings. The third night consisted of the opposite for each patient, either a control-sham or an NPPV night. On the second and third nights, three arterial blood gas readings were obtained: (1) baseline wakefulness; (2) non-rapid eye movement (NREM) sleep; and (3) rapid eye movement (REM) sleep.

Results: During NREM sleep, NPPV in comparison to the control-sham night on low level CPAP caused no significant change in PaCO2 (60±4 to 59±3 mm Hg [p=0.6]) and a decrease in PaO2 (96±9 to 72±5 mm Hg [p=0.04]). During REM sleep, NPPV in comparison to the control-sham night on low level CPAP caused no significant change in either PaCO2 (63±7 to 57±2 mm Hg [p=0.46]) or PaO2 (67±7 to 75±8 mm Hg [p=0.51]). Sleep efficiency and total sleep time (TST) increased significantly with NPPV in comparison to the control-sham night on low level CPAP: from 63±7% to 81±4% (p<0.05) and from 205±32 to 262±28 min (p<0.05), respectively. Sleep architecture, expressed as a percentage of TST, was unchanged on the NPPV night compared to the control-sham night on low level CPAP. The number of arousals during the night was also unchanged with NPPV in comparison to the control-sham night on low level CPAP (45±11 to 42±9 [p=not significant]).

Conclusions: NPPV acutely improved sleep efficiency and TST in patients with hypercapnic COPD without significantly improving gas exchange. Other sleep parameters, including sleep architecture and the number of arousals during the night, remained unchanged during NPPV. These data suggest that the beneficial effects of NPPV in patients with hypercapnic respiratory failure are not solely due to an improvement in gas exchange but may be more complex with other factors potentially having contributing roles.


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