Beachey: Respiratory Care Anatomy and Physiology, 2nd Edition

Answers to Concept Questions

Chapter 15: Fetal and Newborn Cardiopulmonary Physiology

15-1	An infant born prematurely at 24 weeks is capable of breathing. However, the lack of mature surfactant results in high surface tension and alveolar collapse leading to respiratory distress with signs such as nasal flaring, grunting, and intercostal retractions. This increased work of breathing eventually leads to ventilatory failure, which requires mechanical ventilation. Surfactant replacement therapy may alleviate or eliminate these problems.

15-2	Fetal lung fluid is important in maintaining the size, shape, and patency of developing airways. The absence of adequate amounts of fetal lung fluid can lead to underdevelopment of the fetal lung (hypoplastic lung).

15-3	Because the fetus relies on maternal blood flow for gas exchange, any factor that decreases maternal blood flow (e.g., hypertension or chronic hypoxemia) will decrease fetal gas exchange.

15-4	Hemoglobin present in the fetus (HbF) has a high affinity for oxygen. This increase in affinity is associated with a left shift of the fetal oxyhemoglobin dissociation curve, which means that oxygen binds more readily to HbF. This facilitates the placental transfer of oxygen to the fetus and allows the fetus to survive in a relatively hypoxic environment.

15-5	Infants are more prone to airway obstruction than adults for many reasons. The smaller size of the mouth and nose and the smaller diameter of the airways can lead to significant airway narrowing and obstruction in the presence of mucosal edema or secretions in the airways. Moreover, the soft, compliant nature of the airways makes them more prone to compression or collapse, which can also lead to airflow obstruction.

15-6	Cardiac defects such as aortic stenosis and tricuspid atresia result from abnormal development of the atrioventricular and semilunar valves. Atrial and ventricular septal defects may also occur during this period of fetal development.

15-7	Prolonged labor can result in fetal hypoxemia caused by the stress of contractions that last for a long period of time or are of high intensity. Fetal hypoxemia may lead to meconium aspiration and respiratory distress, placing the fetus at high risk for complications associated with delivery.

15-8	Infants experiencing retention of fetal lung fluid have rapid respiratory rates (tachypnea), grunting, intercostal retractions, nasal flaring, and cyanosis within hours of delivery. A chest radiograph shows pulmonary vascular congestion with prominent 
hilar markings and possible fluid in the interlobar fissures. Symptoms and chest x-ray findings gradually clear within 24 to 48 hours following the onset of symptoms.

15-9	If there is a right-to-left shunt through a patent ductus arteriosus (PDA), then the PO2 of radial artery blood would be higher than the PO2 of umbilical artery blood. The ductus arteriosus connects the pulmonary artery with the aorta at a point just distal to the arteries that arise from the aortic arch—arteries that supply the head and upper extremities. Unoxygenated blood shunted from the right side of the heart through a PDA would bypass the lungs and mix with oxygenated blood in the aorta at a point just downstream from the aortic arch; thus blood in the descending aorta—which ultimately supplies the umbilical artery—would have a lower PO2 than blood supplying the head and upper extremities.

15-10	The infant with a hypoplastic left ventricle pumps very little, if any, blood into the aorta. The presence of an atrial septal defect (ASD) and a patent ductus arteriosus (PDA) provides the only pathway for oxygenated blood to reach the aorta and the systemic circulation. Oxygenated blood from the lungs flowing into the left atrium must pass through an ASD into the right atrium; from there it flows into the right ventricle and is pumped into the pulmonary artery, where some of it passes through a PDA into the aorta. A potential complication of oxygen therapy in this condition is that if the blood oxygen level rises sufficiently, it might inhibit the prostaglandins that are responsible for keeping the ductus arteriosus patent. In other words, increased blood oxygen levels could cause the ductus arteriosus to close, eliminating the only pathway for oxygenated blood to pass into the systemic circulation.