A dynamic model for assessing the impact of diffusing capacity on arterial oxygenation during apnea

Preterm infants have a reduced pulmonary diffusing capacity that has been invoked to explain rapid arterial O2-desaturation during apnea, despite little evidence to support this view. We explored the role of diffusion limitation on O2-desaturation during apnea by developing a mathematical model of gas exchange in which O2 dynamically loads the blood traversing the pulmonary capillary. While normal diffusing capacity (DLO2)(DLO2) had negligible impact on apneic desaturation, reduced DLO2DLO2 advanced the onset of desaturation during apnea. Unexpectedly, despite considerable diffusion limitation, its influence on O2-desaturation disappeared within 15 s, because its impact in slowing alveolar O2 depletion maintained a higher driving pressure for diffusion. In contrast, reduced DLO2DLO2 substantially slowed reoxygenation following apnea. Our findings do not support the hypothesis that reduced DLO2DLO2 explains the rapid apneic desaturation observed in preterm infants. Instead, the signature of reduced DLO2DLO2 is a prolonged hypoxemia following apnea, potentially causing a persistence of hypoxic conditions when heart rate and cardiac workload reach a peak.