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Birth involves changes in numerous organ systems in the infant, but only a few require relatively rapid postnatal adjustment. The most important of these birth-related changes involve transitional function in the respiratory, cardiovascular, thermoregulatory, and metabolic systems.

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Within minutes after birth, regular breathing efforts are sustained, lung compliance improves, airway resistance diminishes, and a functional residual capacity is established. With these changes, gas tensions of both oxygen and carbon dioxide in the blood approach those expected in the mature postnatal infant. The physiological triggers for establishing regular breathing efforts are probably the loss of the umbilical circulation and the increase in systemic oxygen content.1-3

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A critical element necessary for pulmonary adaptation after birth is surfactant. Surfactant derives its importance from its ability to lower the surface tension of the alveolar lining layer, the shallow pool of liquid that overlies the cells of the distal airspaces. Without a very low surface tension at end-expiration, the airspaces become atelectatic with exhalation. It is a deficiency of surfactant that underlies the pathophysiology of the respiratory distress observed after premature birth.4

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Surfactant is synthesized in the type II cells that line the distal airspaces. It is composed primarily of lipids, including the disaturated phospholipids, which are responsible for the relevant biophysical properties. Associated with these lipids are a small but critical collection of proteins, the surfactant-associated proteins A, B, C, and D. Proteins B and C are water-insoluble, hydrophobic proteins that are closely associated with the lipid component of surfactant. The pivotal role of these latter 2 proteins is exemplified by respiratory distress syndromes that result from their genetic alteration. Specifically, the absence of surfactant protein B results in severe respiratory failure unresponsive to routine supportive care.5

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During the latter stages of intrauterine development, the enzymes important in surfactant production increase and result in an increase in intracellular surfactant content. At the time of birth, much of this stored surfactant is released into the alveolar space. Surfactant release is stimulated by lung inflation and the increase in circulating catecholamine concentration that accompanies birth. The premature infant has less surfactant available for extrusion into the airspace at the time of birth than does a term infant.6

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In addition to an adequate concentration of surfactant, postnatal lung adaptation also depends on clearance of fluid from the lumen of the lung. Before birth, the potential airspaces are filled with liquid, and failure to remove this liquid after birth results in respiratory difficulty and hypoxemia. Fetal lung liquid is produced by a process that is dependent on the secretion of Cl ions across the respiratory epithelium into the lung lumen. The importance of fetal lung liquid derives from its ability to act as a dynamic template around which the lung develops in utero. If the fetal airspaces are inadequately distended with liquid, lung growth is stunted and lung cell differentiation is disturbed.7

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