Infant respiratory distress syndrome (RDS) occurs in about 1% of deliveries worldwide, but it is most common in preterm infants, and occurs in 75% of babies delivered at 26-28 weeks of gestational age. Infants with RDS have rapid shallow breathing, hypoxemia, and acidosis, and can die without treatment within 72 hr. In 1959, Avery and Mead showed that extracts from infants with RDS had abnormal surface tension. This led to our current understanding of RDS as a disease resulting primarily from abnormal surfactant and to our current treatments with surfactant replacement.
Surfactant production normally begins in utero and term infants are born with lung surfactant levels greater than adults. Such high surfactant levels probably help protect the airway epithelium from damage by high shear forces from amniotic fluid during breathing movements in utero, and improve lung mechanics during the transition from fluid to air breathing upon birth. Normal surfactant metabolism is assured only after 36 weeks' gestation, and preterm infants appear to suffer from surfactant dysfunction as much as surfactant deficiency. The normal cycle of lamellar body secretion, formation of tubular myelin, and adsorption of surfactant to the alveolar surfaces does not occur until after full-term birth. Hyaline membranes, or a coagulation of cellular debris and plasma proteins, line the alveoli in infant RDS, which is also known as hyaline membrane disease.
Surface tension is high with RDS, so normal inflation pressures of 5-10 cm H2O are ineffective at expanding the lung. The stiff lung of RDS and the compliant chest wall of the newborn decrease FRC. RDS infants breathe with an expiratory grunt, by contracting the vocal cords during expiration to maintain lung volume. These factors increase the work of breathing and can lead to a metabolic acidosis. Rapid shallow breathing increases dead space ventilation. Abnormal surfactant also leads to hypoxemia from edema and atelectasis (alveolar collapse) by increasing alveolar surface tension, and probably by changing epithelial permeability.
Surfactant replacement therapy has increased infant RDS survival from 30% in the 1970s to 90% today. Exogenous surfactant can be instilled in the trachea and it spreads into the lungs and alveoli during artificial ventilation. Surfactant can be isolated from late gestational human amniotic fluid or animal lungs, synthesized in the laboratory, or produced from bacteria using genetic engineering. Synthesizing surfactant that contains the normal apoproteins may be important for correcting defects other than increased surface tension, and the genetic engineering approach holds the most promise for therapies in other forms of RDS, such as acute RDS in adults.
lung. Total respiratory system is a function of pressure in the closed airway during relaxation at any volume. (At FRC, the airway can be open because FRC is by definition the relaxed lung volume.) Chest wall behavior is calculated as the difference between the respiratory system and lung curves, both of which can be measured physiologically. In theory, the chest wall curve could be measured by positive pressure inflation of an empty thoracic cage.
FRC occurs at the end of a normal expiration when respiratory system transmural pressure (Prs) is zero. Figure 6 shows how this results from an interaction between the lung and chest wall so transmural pressure across the lung (Pl) and chest wall (Pw) are equal and opposite at FRC. The tendency for the lung to collapse is perfectly balanced by the tendency for the chest wall to expand at FRC. At volumes below FRC, the chest wall tends to expand even more. Residual volume (RV) occurs when the expiratory muscles cannot generate sufficient force to decrease volume further. Figure 6 shows that RV is greater than the minimal volume of the lung (MV). MV includes gas in large stiff airways and gas trapped in alveoli distal to small collapsed airways. The lungs can never reach MV in an intact respiratory system but a pneumothorax, or leak between the intrapleural space and atmosphere, can cause total deflation of the lungs and seriously compromise gas exchange. A pneumothorax eliminates the subatmo-spheric Ppl that holds the lungs open.
At high lung volumes, the chest wall has a tendency to collapse. Therefore, a positive Prs is necessary across both the lung and chest wall to achieve high lung volumes. Total pressure to inflate the respiratory system increases as the sum of lung and chest wall pressures (Prs = Pl + Pw). TLC occurs at the elastic limits of the chest wall, but this is also very near the limits of the lungs. Lung compliance decreases sharply at high volumes (see Figs. 3 and 6), so volume could not
19. Mechanics of Breathing tlc
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