August 2002 / Volume 47 / Number 8 / Page 882
Are Daytime Arterial Blood Gases a Good Reflection of Nighttime Gas Exchange in Patients on Long-Term Oxygen Therapy?
IntroductionOBJECTIVE: Compare nighttime and daytime arterial blood gas values in patients undergoing long-term oxygen therapy (LTOT). METHODS: We studied 39 LTOT patients with chronic airflow limitation. Oxygen from an oxygen concentrator was administered via nasal prongs until daytime blood oxygen saturation (measured via pulse oximetry [SPO2]) was > or = 90%. Arterial blood samples were drawn at 6:00 pm, while the subject breathed room air, and also during oxygen administration at night (3:00 am), early in the morning (7:00 am), and at noon. SPO2 was measured throughout the night. RESULTS: Mean patient age was 70 ± 7 yr. All patients suffered severe chronic airflow limitation (mean forced expiratory volume in the first second 28 ± 9% of predicted). The mean oxygen flow administered was 1.41 ± 0.6 L/min. Mean overnight SPO2 was 92 ± 2.5%, with 21.5 ± 28% of recording time under 90%. There were statistically significant differences between PaO2, PaCO2, and pH obtained at 3:00 am and noon and between 7:00 am and noon, while the patients breathed the same oxygen concentration. The differences between the 3:00 and 7:00 am values were not significant. In 23 patients (59%) we observed a PaCO2 increase > 10 mm Hg and/or a pH decrease to < 7.33 during that period, indicating poor response to LTOT. CONCLUSIONS: Daytime arterial blood gas measurements do not reflect nighttime gas exchange. However, samples taken early in the morning (7:00 am) do seem to reflect arterial blood gases during the night and can therefore be used for setting and monitoring nighttime oxygen flow.
Diaphragmatic Breathing and Huffing
Active Cycle of Breathing Technique
Positive Expiratory Pressure Therapy
High-Frequency Chest Wall Oscillation
Oscillating Positive Expiratory Pressure
Long-term oxygen therapy (LTOT) improves measures of pulmonary hemodynamics in patients with chronic obstructive pulmonary disease (COPD) and lengthens the survival of patients with both COPD and chronic respiratory failure. It is generally believed that oxygen can provide the same benefits to patients with respiratory failure due to diseases other than COPD, such as bronchiectasis, pulmonary fibrosis, cystic fibrosis, or tuberculosis sequelae, although well-designed studies that support that hypothesis are lacking.
See The Related Editorial on Page 876
According to widely accepted guidelines, oxygen flow to correct hypoxemia is titrated based on daytime arterial blood gas (ABG) values or oxyhemoglobin saturation. A nighttime oxygen flow increase of 1 L/min more than the daytime flow is recommended to avoid nighttime desaturation. However, substantial changes in ventilation and gas exchange take place during sleep. Oxygen therapy mitigates nocturnal desaturation, but studies of transcutaneously measured PCO2 suggest that hypoventilation and consequent hypercapnia may develop. Such reports suggest that current methods for titrating nighttime oxygen flow might not be optimal, although studies of nighttime ABG values in these patients are lacking. Recently, in a small sample of sleeping patients receiving LTOT for severe airflow obstruction due to cystic fibrosis, Milross et al measured ABG values and found that nighttime PaCO2 increased significantly and pH decreased.
Our hypothesis for the present study was that a considerable proportion of patients receiving oxygen therapy develop substantial hypercapnia and respiratory acidosis during sleep, even though daytime ABG values appear to indicate that oxygen flow has been appropriately titrated. To test this hypothesis we compared nighttime and daytime ABG values in patients undergoing oxygen therapy.