A Model Analysis of Arterial Oxygen Desaturation during Apnea in Preterm Infants

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Abstract
Rapid arterial O2 desaturation during apnea in the preterm infant has obvious clinical implications but to date no adequate explanation for why it exists. Understanding the factors influencing the rate of arterial O2 desaturation during apnea ( ) is complicated by the non-linear O2 dissociation curve, falling pulmonary O2 uptake, and by the fact that O2 desaturation is biphasic, exhibiting a rapid phase (stage 1) followed by a slower phase when severe desaturation develops (stage 2). Using a mathematical model incorporating pulmonary uptake dynamics, we found that elevated metabolic O2 consumption accelerates throughout the entire desaturation process. By contrast, the remaining factors have a restricted temporal influence: low pre-apneic alveolar causes an early onset of desaturation, but thereafter has little impact; reduced lung volume, hemoglobin content or cardiac output, accelerates during stage 1, and finally, total blood O2 capacity (blood volume and hemoglobin content) alone determines during stage 2. Preterm infants with elevated metabolic rate, respiratory depression, low lung volume, impaired cardiac reserve, anemia, or hypovolemia, are at risk for rapid and profound apneic hypoxemia. Our insights provide a basic physiological framework that may guide clinical interpretation and design of interventions for preventing sudden apneic hypoxemia. When breathing stops, the flow of O2 into and the flow of CO2 out of the body cease. Such an event, termed an apnea, can be especially dangerous in preterm infants in whom it can lead to a rapid decline in arterial O2 saturation, reaching rates of 3–8% per second, rapidly reducing O2 to a level that could lead to neurological damage. Despite extensive experimental research, we have a poor mechanistic understanding of the causes of rapidly developing hypoxemia. We describe a new mathematical model that allows examination of the importance of the major cardiorespiratory factors that are likely to influence the speed at which arterial hypoxemia worsens during apnea. We found that high metabolic rate as well as reduced pre-apneic ventilation, lung volume, cardiac output, hemoglobin content, blood O2 affinity, and blood volume accelerate the development of hypoxemia during apnea. Importantly, the cardiorespiratory factors that contribute to rapid hypoxemia are all pertinent to the preterm infant during early postnatal development. Thus the newborn is highly susceptible to rapid and severe desaturation, potentially explaining the propensity of preterm infants, particularly those with apnea, to neurological impairment.