MECHANISM OF TRANSIENT NOCTURNAL HYPOXEMIA IN HYPOXIC CHRONIC-BRONCHITIS AND EMPHYSEMA

In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls > 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 .+-. 1.9 (SD) Torr during the HE (P < 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 .+-. 2.4 Torr (P > 0.4). The arteriovenous O2 content difference fell by 0.64 .+-. 0.43 ml/100 ml of blood during the HE (P < 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 .+-. 5.6 Torr (P < 0.05), but mean PaCO2 rose by only 2.8 .+-. 2.1 Torr (P > 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.