Sleep fragmentation, decreased rapid eye movement (REM) sleep time, an
d REM sleep hypoxemia have been reported in infants with chronic neona
tal lung disease (CNLD) in early infancy despite an awake hemoglobin o
xygen saturation (SaO(2)) >93%. Interestingly, higher inspired O-2 con
centrations have been demonstrated to reduce REM sleep fragmentation i
n CNLD patients in middle infancy. However, the effect of increased Sa
O(2) on sleep architecture in infants with CNLD near the time of disch
arge from neonatal intensive care has not been reported. We performed
paired overnight polysomnography in a sleep laboratory on 16 infants w
ith CNLD (4 weeks median corrected age) in air or their usual inspired
oxygen (SaO(2) >93%) and again when receiving 0.25 L/min higher than
baseline inspired oxygen via nasal catheters (SaO(2) >97%). A control
group of seven healthy preterm infants was similarly studied. For CNLD
infants on supplemented O-2, sleep duration decreased by 15% (422 +/-
66 min vs. 359 +/- 89 min; P < 0.005), and sleep efficiency decreased
by 7% (73.2 +/- 10.6% vs. 66.4 +/- 14.0%; P < 0.005) but percentage o
f time in REM sleep (REM%) (31.5 +/- 8.9% vs. 29.8 +/- 8.6%; P = 0.560
), REM epoch duration (12.4 +/- 2.8 min vs. 13.4 +/- 4.3 min; P = 0.42
0), and REM arousal index (18.6 +/- 6.5 vs. 18.8 +/- 7.2; P = 0.990) w
ere not significantly affected. Conversely, higher O-2 did not alter s
leep architecture in the control group. The mean non-REM (NREM) respir
atory rate decreased (CNLD: P = 0.003; controls: P = 0.02), NREM SaO(2
) increased (P < 0.05), although the mean transcutaneous CO2 was unalt
ered in both CNLD and control groups. This study confirmed low REM% in
CNLD infants in early infancy and demonstrated that a higher SaO(2) a
dversely affected sleep time but did not influence REM sleep duration
or arousal frequency. A target SaO(2) >93% is, therefore, as efficacio
us as an SaO(2) >97% in optimizing sleep architecture in CNLD infants.
Pediatr Pulmonol, 1998; 26:235-240, (C) 1998 Wiley-Liss, Inc.