Chest
Volume 89, Issue 1, January 1986, Pages 30-38
Journal home page for Chest

Clinical Investigations
Acute Oxygen in Patients with Sleep Apnea and COPD

https://doi.org/10.1378/chest.89.1.30Get rights and content

Nocturnal oxygen administered to patients with disordered breathing ameliorates hypoxemia. As a result, an important chemical stimulus to arousal is diminished. This could cause prolongation of disordered breathing events, worsen respiratory acidosis, and induce potentially harmful cardiac arrhythmias. The presence of chronic obstructive pulmonary disease (COPD) could further aggravate the situation since such patients may have depressed hypercarbic responses. To test this hypothesis, 20 obese men with sleep apnea and COPD were studied polysomnographically on two nights receiving air on one or oxygen at 4 L/min on the other. Supplemental oxygen increased mean DOB event duration from 25.7 to 31.4 seconds (p<0.001), increased end apneic Pco2 from 52.8 to 62.3 mm Hg (p<0.025), and decreased mean end apneic pH from 7.34 to 7.28 (p<0.001). At the same time, it improved mean sleeping and end-apneic oxygen saturation. The number of ventricular extrasystoles (PVCs) per minute of sleep showed small increases in three subjects while breathing oxygen. Complex ventricular arrhythmias were unaffected by oxygen in five subjects. Oxygen eliminated atrioventricular block in two subjects. We conclude that nocturnal supplemental oxygen does not increase ventricular arrhythmias in the majority of patients with COPD and coexisting disordered breathing events. While the clinical significance of an oxygen associated increase in ventricular extrasystoles in three subjects is unclear, nocturnal monitoring by telemetry or ambulatory recorder should be sufficient to detect such patients.

Section snippets

Patient Population

We studied 20 men with previously established diagnosis of sleep apnea and COPD seen by the pulmonary service of the Houston Veterans Administration Medical Center between September 1982 and April 1984. Their mean age was 56.8 years, and all were obese (mean IBW = 162 percent ± 24). All subjects were cigarette smokers, (mean 71.3 pack years), and had symptoms or signs compatible with COPD, including chronic cough, dyspnea on exertion, or expiratory wheezing. Pulmonary function tests were

Results

Average disordered breathing event index (events per hour of sleep) for the group was 88.2 (±27) per hour of which 68 percent were apneas and 32 percent hypopneas. Eighteen subjects had right heart failure with chronic peripheral edema and right ventricular ejection fractions less than 45 percent. Since three of these also had left ventricular ejection fractions less than 50 percent, the diagnosis of cor pulmonale was made in only 15 subjects (Table 1). Results of pulmonary function tests are

Discussion

The purpose of this study was to monitor the cardiopulmonary effects of nocturnal oxygen in COPD patients with substantial numbers of sleep-related disordered breathing events. We believe that this issue is relevant to modern therapy since recent publications demonstrating the efficacy of home oxygen for hypoxemic COPD patients will undoubtedly lead to its wider use. The strong association of male sex, obesity, and age with disordered breathing10 and the recently described high prevalence of

REFERENCES (24)

  • AP Fishman

    Chronic cor pulmonale

    Am Rev Respir Dis

    (1976)
  • A Rechtschaffen et al.

    A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects

    (1968)
  • Cited by (62)

    • Oxygen Therapy in Sleep-Disordered Breathing

      2021, Chest
      Citation Excerpt :

      NSO may be indicated when significant nocturnal hypoxia persists in patients with COPD despite optimal pharmacotherapy without seemingly increasing the risk of hypercapnia.20,44 However, oxygen may suppress the hypoxic respiratory drive, and as such, may contribute to prolonged duration of apnea in patients with OSA.18,19,25,45 In turn, this could lead to hypercapnia and acidosis in patients with OSA, especially in the setting of comorbid obstructive lung disease or hypoventilation.

    • Hypoxia in the pediatric sleep lab: what (not) to do?

      2020, Sleep Medicine
      Citation Excerpt :

      One can therefore assume that blunting of the hypoxic arousal response was the predominant factor causing this increase and that due to prolonged obstruction, CO2 levels increased during sleep. This increased duration of obstructive events due to supplemental oxygen has been previously described in adults with OSA and COPD and in other OSA patients as well [1,2]. On the other hand, infants with OSA can be succesfully treated with supplemental oxygen but this might be due to physiological differences in ventilatory control [3].

    View all citing articles on Scopus

    This investigation was supported in part by a grant from the Texas Affiliate of the American Heart Association and the General Medical Research Service of the Veterans Administration.

    Manuscript received March 11; revision accepted July 16.

    View full text