Chest
Volume 92, Issue 4, October 1987, Pages 604-608
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Clinical Investigations
Nocturnal Oxyhemoglobin Desaturation in COPD Patients with Arterial Oxygen Tensions Above 60 mm Hg

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We studied 152 COPD patients with a daytime PaO2≥60 mm Hg using formal polysomnography (EEG, airflow, respiratory muscle movement, ear oximeter) to detect the presence of nocturnal, nonapneic, oxyhemoglobin desaturation. Nine subjects were disqualified by the unexpected discovery of sleep apnea, as were another eight because they could not sleep in the laboratory setting. Of the remaining 135 subjects, 37 (27 percent) desaturated below a baseline sleep saturation of 90 percent for five minutes or more, reaching a nadir saturation of at least 85 percent. Anthropomorphic, pulmonary function, and historic factors comparing desaturators and nondesaturators failed to separate the groups. Awake PaO2 at rest in the desaturators was significantly lower than in the nondesaturators. The PaCO2 was higher in the desaturators. Reversibility of the desaturation phenomenon was demonstrated in three patients during subsequent polysomnographic studies following periods of clinical improvement. Continuous oxyhemoglobin monitoring during sleep remains the only reliable tool for detecting nocturnal desaturation.

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MATERIALS AND METHODS

We studied 152 male United States veterans from a medical chest clinic with the diagnosis of COPD using nocturnal polysomnography to detect oxyhemoglobin desaturation. Requirements for inclusion were as follow: (1) a clinical diagnosis of COPD characterized by symptoms of chronic cough, exertional dyspnea, or wheezing; (2) spirometry consistent with irreversible expiratory airflow obstruction (FEV1<80 percent predicted, FEV1/FVC<0.75) or evidence of airtrapping on body plethysmography; and (3)

RESULTS

Eight subjects were disqualified because of inability to achieve or maintain adequate sleep (more than one to two hours of NREM sleep) for sleep stage and SaO2 analysis. Most of these were studied on two or more occasions. Nine were disqualified because of the presence of five or more obstructive apneas per hour in spite of the absence of clinical symptoms of sleep apnea. Thirty seven (27 percent) of the remaining 135 subjects showed nocturnal oxyhemoglobin desaturation as described above (Fig 1

DISCUSSION

Transient oxygen desaturation in chronic lung disease probably results from a combination of alveolar hypoventilation and gas exchange abnormalities contributed to by REM sleep muscular atonia and changes in respiratory control.20, 21, 22 Attention has been given to the role of transient alveolar hypoxia and hypoxic vasoconstriction as possible causes of sustained pulmonary hypertension.13, 14 Several authors23, 24, 25, 26 have demonstrated that repetitive episodes of transient hypoxia in

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  • Cited by (0)

    This study was supported by the General Research Service of the Veterans Administration. Computational assistance was provided by the CLINFO project, funded by the Division of Research Resources of the NIH under grant RR-00350.

    Manuscript received December 29; revision accepted February 12.

    Medical Center, 2002 Holcombe Blvd, Houston 77211

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