Prematurity, the diagnosis of bronchopulmonary dysplasia, and maturation of ventilatory control.

Abstract

Infants born before 32 weeks gestational age and receiving respiratory support at 36 weeks postmenstrual age (PMA) are diagnosed with bronchopulmonary dysplasia (BPD). This label suggests that their need for supplemental oxygen (O2 ) is primarily due to acquired dysplasia of airways and airspaces, and that the supplemental O2 is treating residual parenchymal lung disease. However, emerging evidence suggests that immature ventilatory control may also contribute to the need for supplemental O2 at 36 weeks PMA. In all newborns, maturation of ventilatory control continues ex utero and is a plastic process. Among premature infants, supplemental O2 mitigates the hypoxemic effects of delayed maturation of ventilatory control, as well as reduces the duration and frequency of periodic breathing events. Nevertheless, prematurity is associated with altered and occasionally aberrant maturation of ventilatory control. Infants born prematurely, with or without a diagnosis of BPD, are more prone to long-lasting effects of dysfunctional ventilatory control. This review addresses normal and abnormal maturation of ventilatory control and suggests how aberrant maturation complicates assigning the diagnosis of BPD. Greater awareness of the interaction between parenchymal lung disease and delayed maturation of ventilatory control is essential to understanding why a given premature infant requires and is benefitting from supplemental O2 at 36 weeks PMA.