Although the airways and alveoli of a neonate’s respiratory system are present by the 27th week of gestation, the intercostal muscles are weak and the alveoli and capillary blood supply are immature. In respiratory distress syndrome, the premature neonate develops widespread alveolar collapse because of lack of surfactant, a lipoprotein present in alveoli and respiratory bronchioles.

Surfactant normally lowers surface tension and aids in maintaining alveolar patency, preventing collapse, particularly at end expiration. But a deficiency results in widespread atelectasis, which leads to inadequate alveolar ventilation with shunting of blood through collapsed areas of lung, causing hypoxia and acidosis.

Although a neonate with respiratory distress syndrome may breathe normally at first, he usually develops rapid, shallow respirations within minutes or hours of birth, with intercostal, subcostal, or sternal retractions; nasal flaring; and audible expiratory grunting. This grunting is a natural compensatory mechanism designed to produce positive end-expiratory pressure (PEEP) and prevent further alveolar collapse.