Mechanism underlying accelerated arterial oxygen desaturation during recurrent apnea.
BACKGROUND
Brief recurrent apneas in preterm infants and adults can precipitate rapid and severe arterial O(2) desaturation for reasons that remain unclear.


OBJECTIVE
We tested a mathematically derived hypothesis that when breathing terminates apnea, mixed-venous hypoxemia continues into the subsequent apnea; as a result, there is a surge in pulmonary O(2) uptake that rapidly depletes the finite alveolar O(2) store, thereby accelerating arterial O(2) desaturation.


METHODS
Recurrent apneas were simulated in an experimental lamb model. Pulmonary O(2) uptake was calculated from continuously measured arterial and mixed-venous O(2) saturation and cardiac output.


RESULTS
Direct measurements revealed that asynchrony in the desaturation and resaturation of arterial and venous blood gave rise to dips and surges in O(2) uptake. After desaturation to 50%, a typical nadir in preterm infants, O(2) uptake surged to a peak of 176.9 ± 7.8% of metabolic rate. During subsequent apneas, desaturation rate was increased two- to threefold greater than during isolated apneas, in direct proportion to the magnitude of the surge in O(2) uptake (P < 0.001; R(2) = 0.897). Application of our mathematical model to a published recording of cyclic apneas in a preterm infant precisely reproduced the accelerated desaturation rates of up to 15% · s(-1) observed clinically.


CONCLUSIONS
Rapid depletion of alveolar O(2) stores by surges in O(2) uptake almost completely explains the acceleration of desaturation that occurs during recurrent apnea. This powerful mechanism is likely to explain the severity of intermittent hypoxemia that is associated with neurocognitive and cardiovascular morbidities in preterm infants and adults.
Sands
Scott A
SA
The Ritchie Centre Monash Institute of Medical Research, Monash University, Melbourne, Victoria, Australia.
Edwards
Bradley A
BA
Kelly
Vanessa J
VJ
Skuza
Elizabeth M
EM
Davidson
Malcolm R
MR
Wilkinson
Malcolm H
MH
Berger
Philip J
PJ
D000818:Animals; D000831:Animals, Newborn; D001049:Apnea / Q000503:physiopathology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D007231:Infant, Newborn; D007234:Infant, Premature; D016014:Linear Models; D008954:Models, Biological; D010108:Oxyhemoglobins / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000098:blood supply; D011659:Pulmonary Gas Exchange; D012008:Recurrence; D012756:Sheep
D010108:Oxyhemoglobins