[Frequency and severity of hypoxemia during sleep in COPD. Clinical and therapeutic impact]

The occurrence of episodes of desaturation during sleep in patients suffering from chronic airflow obstruction is well known. The severity of nocturnal hypoxaemia depends, in part, on the level of the diurnal PaO2. Hypoventilation linked to sleep is the principle mechanism responsible for the decrease in PaO2 and the desaturation which results and depends on the level of oxyhaemoglobin saturation (SaO2) during wakefulness. However, it is not possible to predict the severity of nocturnal desaturation solely on the basis of diurnal oxyhaemoglobin saturation. Numerous factors may contribute to a worsening of nocturnal desaturation. In some patients it may be associated with hypoventilation and a worsening of the ventilation perfusion inequalities. A fall in the ventilatory response to hypoxaemia and hypercapnea contributes equally to the severity of desaturation. The awake response to hypoxia is variable according to the stage of their respiratory failure but may play a role in worsening nocturnal hypoxia. Snoring and obstructive apnoea are responsible for severe desaturation in chronic airflow obstruction presenting as hypoxaemia which may be moderated during the day. At present the value of systematic nocturnal polygraphic recordings in the "work-up" of chronic airflow obstruction has not been demonstrated. Its principle practical interest is in research into the associated sleep apnoea syndrome. It should be recognised in a patient with chronic airflow obstruction who snores and is somnolent with hypoxaemia and/or poorly explained hypercapnea. The therapeutic approach in respiratory failure should take account of nocturnal desaturation and the oxygen flow at night should be superior to the one to two litres which are required to correct the diurnal hypoxaemia.