TY - JOUR
T1 - The effect of chronic nocturnal oxygen administration upon sleep apnea
AU - Gold, A. R.
AU - Schwartz, A. R.
AU - Bleecker, E. R.
AU - Smith, P. L.
PY - 1986
Y1 - 1986
N2 - Administration of nocturnal oxygen for 1 night to patients with obstructive sleep apnea (OSA) causes a moderate reduction in apnea frequency without improving hypersomnolence. Therefore, we administered oxygen chronically to patients with OSA to determine: (1) whether apnea frequency would be further reduced, (2) whether the effect of oxygen upon apnea frequency is correlated with an increased ventilatory response to hypoxia and hypercapnia, and (3) whether hypersomnolence improves with more prolonged oxygen administration. In a single-blinded, nonrandomized trial, we compared the effects of 1 month of oxygen (4 L/min by nasal cannula) with room air (4 L/min by nasal cannula) placebo during sleep in 7 men and 1 woman with obstructive sleep apnea. During non-REM sleep, acute oxygen administration elevated the average low oxy-hemoglobin saturation during apneic events and decreased apnea frequency. These acute effects persisted during chronic oxygen administration but reverted to the preoxygen effects immediately upon discontinuing oxygen. One month of oxygen did not affect the waking ventilatory response to hypoxia or hypercapnia; however, waking Pa(CO2) increased from 40 ± 1 mm Hg (mean ± SE) after placebo to 43 ± 1 mm Hg after oxygen (p < 0.01). Neither subjective nor objective hypersomnolence consistently improved after 1 month of oxygen administration. We conclude that: first, oxygen has no effect upon apnea frequency beyond the period of administration, and the reduction of apnea frequency is not correlated with an increased sensitivity to chemical ventilatory stimuli. The reduced apnea frequency may be related to an increased Pa(CO2) stimulating ventilation during sleep. Second, the absence of an improvement in daytime sleepiness after chronic oxygen administration suggests that other factors (i.e., recurrent arousals, hypercapnia) are more important determinants of hypersomnolence. Alternatively, factors associated with oxygen administration (i.e., increased CO2 retention) may worsen sleepiness and mask an effect of oxygen upon this symptom.
AB - Administration of nocturnal oxygen for 1 night to patients with obstructive sleep apnea (OSA) causes a moderate reduction in apnea frequency without improving hypersomnolence. Therefore, we administered oxygen chronically to patients with OSA to determine: (1) whether apnea frequency would be further reduced, (2) whether the effect of oxygen upon apnea frequency is correlated with an increased ventilatory response to hypoxia and hypercapnia, and (3) whether hypersomnolence improves with more prolonged oxygen administration. In a single-blinded, nonrandomized trial, we compared the effects of 1 month of oxygen (4 L/min by nasal cannula) with room air (4 L/min by nasal cannula) placebo during sleep in 7 men and 1 woman with obstructive sleep apnea. During non-REM sleep, acute oxygen administration elevated the average low oxy-hemoglobin saturation during apneic events and decreased apnea frequency. These acute effects persisted during chronic oxygen administration but reverted to the preoxygen effects immediately upon discontinuing oxygen. One month of oxygen did not affect the waking ventilatory response to hypoxia or hypercapnia; however, waking Pa(CO2) increased from 40 ± 1 mm Hg (mean ± SE) after placebo to 43 ± 1 mm Hg after oxygen (p < 0.01). Neither subjective nor objective hypersomnolence consistently improved after 1 month of oxygen administration. We conclude that: first, oxygen has no effect upon apnea frequency beyond the period of administration, and the reduction of apnea frequency is not correlated with an increased sensitivity to chemical ventilatory stimuli. The reduced apnea frequency may be related to an increased Pa(CO2) stimulating ventilation during sleep. Second, the absence of an improvement in daytime sleepiness after chronic oxygen administration suggests that other factors (i.e., recurrent arousals, hypercapnia) are more important determinants of hypersomnolence. Alternatively, factors associated with oxygen administration (i.e., increased CO2 retention) may worsen sleepiness and mask an effect of oxygen upon this symptom.
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U2 - 10.1164/arrd.1986.134.5.925
DO - 10.1164/arrd.1986.134.5.925
M3 - Article
C2 - 3096178
AN - SCOPUS:0022996486
SN - 0003-0805
VL - 134
SP - 925
EP - 929
JO - American Review of Respiratory Disease
JF - American Review of Respiratory Disease
IS - 5
ER -