Apnea, hypoxemia, and aborted sudden infant death syndrome.
To find out whether there is any relationship between the ventilatory response to hypoxia and the sudden infant death syndrome (SIDS), we studied the effects of mild induced hypoxia (PIO2, 120 mm Hg = 17% oxygen) in 16 infants aged 2 weeks to 6 months. Eight had recurrent apneic spells (apnea group) (five had aborted SIDS and three had recurrent apnea in the intensive care nursery) and eight were "well" preterm infants about to fly in a pressurized airplane (PIO2, 120 mm Hg) (control group). Mean birth weights were 2,245 and 1,400 gm and mean gestational ages were 35 and 30 weeks. Postconceptual ages (41.8 and 41.3 weeks) were almost identical. Heart rate was obtained from an ECG, and respiratory rate and pattern were obtained from a pneumogram. In addition, end-tidal PCO2 and PN2 or PO2 were obtained with a nasal catheter and gas analyzers. In the apnea group with inhalation of 17% oxygen, we observed an increase in periodic breathing and an increase in both rate and total duration of respiratory pauses. In the control group there were no significant changes. Heart rate and PCO2 did not change in either group. Our findings suggest that infants prone to apnea may have unique respiratory responses to mild induced hypoxia.
D001049:Apnea / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000097:blood; D005260:Female; D006339:Heart Rate; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D012119:Respiration; D013398:Sudden Infant Death / Q000517:prevention & control*
D002245:Carbon Dioxide; D010100:Oxygen