E. Weitzenblum et al., SLEEP-RELATED HYPOXEMIA IN CHRONIC OBSTRUCTIVE PULMONARY-DISEASE - CAUSES, CONSEQUENCES AND TREATMENT, Respiration, 64(3), 1997, pp. 187-193
Worsening of hypoxaemia during sleep in patients with chronic obstruct
ive pulmonary disease has been extensively investigated in the past 20
years owing to the development of polysomnography and to the advent o
f reliable transcutaneous oxymeters. Sleep-related hypoxaemia is chara
cteristic of rapid-eye-movement (REM) sleep but may be present during
other sleep stages. There is a strong relationship between nocturnal O
-2 saturation and the level of daytime PaO2: the more pronounced dayti
me hypoxaemia, the more severe nocturnal hypoxaemia. Sleep-related hyp
oxaemia is due to a variable combination of alveolar hypoventilation a
nd ventilation-perfusion mismatching, alveolar hypoventilation being t
he preponderant mechanism during REM sleep. The deleterious effects of
sleep-related hypoxaemia include cardiac arrhythmias, 'hypoxaemic str
ess' on the coronary circulation and, especially, peaks of pulmonary h
ypertension. The treatment of nocturnal hypoxaemia is conventional O-2
therapy (both nighttime and daytime) in patients who exhibit marked d
aytime hypoxaemia (PaO2 < 55-60 mm Hg). At present data are not suffic
ient for justifying the use of isolated nocturnal O-2 therapy in patie
nts with nocturnal desaturation who do not qualify for conventional O-
2 therapy.