a ground-glass appearance and air bronchogram on the chest X-ray. Finally, because the baby Pao2 was less than 45 torr shortly after birth, the ductus arteriosus remained patent, producing the syndrome known as persistent pulmonary hypertension of the neonate (PPHN). As the infant's condition improved and his PaO2 increased, the ductus arteriosus closed and the signs and symptoms associated with PPHN disappeared. At the time of this writing, the baby was a perfectly normal 3 year-old boy who was attending half-day preschool sessions 5 days per week. 1. In this case, what are the major anatomic alterations of the lung associated with the respiratory disease that developed in the infant? 2. Describe the pathophysiology that develops as the conditions listed in question 1 worsen. 3. Describe how the following conditions are manifested in the clinical setting: Decreased pulmonary diffusion: Decreased lung compliance: 4. Why did PPHN develop in the infant in this case? How did this condition improve? Discussion This case illustrater the possible adverse effects of a premature birth on the infant's alveolar-apillary gas exchange units and pulmonary circulation. During fetal development, the alveolar-capillary system and the quantity of pulmonary surfactant usually are not sufficient to support life until the 28th week of gestation or beyond. In this case, the baby was born at the very beginning of this time period. Thus, because of the immaturity of the baby's alveolar- capilary system, the ability of the type II cells to produce pulmonary surfactant was inadequate. As a result of the insufficient amount of pulmonary surfactant, the pathologic processes of a common newborn respiratory disorder called respiratory distress syndrome (RDS) developed. The anatomic alterations of the lungs associated with RDS indude interstitial and intra-alveolar edema and hemorrhage, alveolar consoldation, intra-alveolar hyaline membrane formation, and atelectasis. All of these pathologic processes cause the alveolar-capillary membranes thickness to increase. As this condtion progressively worsened, the diffusion of oxygen between the alveoli and the pulmonary capillary blood decreased, and the infant's lung compliance decreased. Clinically, the decreased diffusion of oxygen was manifested by cyanosis, increased respiration rate and heart rate, and decreased Pa. The decreased lung compliance was manifested by nasal flaring, intercostal retractions, exhalation grunting, bilateral crackles, and.

1. a ground-glass appearance and air bronchogram on the chest X-ray.
Finally, because the baby Pao2 was less than 45 torr shortly after birth, the ductus arteriosus
remained patent, producing the syndrome known as persistent pulmonary hypertension of the
neonate (PPHN). As the infant's condition improved and his PaO2 increased, the ductus
arteriosus closed and the signs and symptoms associated with PPHN disappeared. At the time of
this writing, the baby was a perfectly normal 3 year-old boy who was attending half-day
preschool sessions 5 days per week.
1. In this case, what are the major anatomic alterations of the lung associated with the respiratory
disease that developed in the infant?
2. Describe the pathophysiology that develops as the conditions listed in question 1 worsen.
3. Describe how the following conditions are manifested in the clinical setting:
Decreased pulmonary diffusion:
Decreased lung compliance:
4. Why did PPHN develop in the infant in this case? How did this condition improve?
Discussion This case illustrater the possible adverse effects of a premature birth on the infant's
alveolar-apillary gas exchange units and pulmonary circulation. During fetal development, the
alveolar-capillary system and the quantity of pulmonary surfactant usually are not sufficient to
support life until the 28th week of gestation or beyond. In this case, the baby was born at the
very beginning of this time period. Thus, because of the immaturity of the baby's alveolar-
capilary system, the ability of the type II cells to produce pulmonary surfactant was inadequate.
As a result of the insufficient amount of pulmonary surfactant, the pathologic processes of a
common newborn respiratory disorder called respiratory distress syndrome (RDS) developed.
The anatomic alterations of the lungs associated with RDS indude interstitial and intra-alveolar
edema and hemorrhage, alveolar consoldation, intra-alveolar hyaline membrane formation, and
atelectasis. All of these pathologic processes cause the alveolar-capillary membranes thickness to
increase. As this condtion progressively worsened, the diffusion of oxygen between the alveoli
and the pulmonary capillary blood decreased, and the infant's lung compliance decreased.
Clinically, the decreased diffusion of oxygen was manifested by cyanosis, increased respiration
rate and heart rate, and decreased Pa. The decreased lung compliance was manifested by nasal
flaring, intercostal retractions, exhalation grunting, bilateral crackles, and