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PERINATAL CARDIORESPIRATORY PHYSIOLOGY

The fetal lung arises from the foregut at 24 days' gestation. By 20 weeks, the airways are lined with cuboidal epithelium, and pulmonary capillaries are present. By 26 to 28 weeks, the capillaries are closely approximated to the developing terminal airways. Between 30 and 32 weeks' gestation, the cuboidal epithelium flattens and thins,^[3] a process that is accelerated by administering prenatal steroids to the mother.^[4] By 20 weeks' gestation, surface active material (SAM) is present within the alveolar lining cells,^[5] and by 28 to 32 weeks' gestation, SAM is present within the lumen of the airways. Significant amounts of SAM do not appear in terminal airways until 34 to 38 weeks' gestation, unless SAM production and release are stimulated by stress or steroids. At birth, the onset of respiration further increases the alveolar concentration of SAM.^[6] Administration of calf, human, or artificial SAM decreases the incidence of hyaline membrane disease and the incidence of serious cardiopulmonary complications in neonates. ^[7] Administration of SAM has become a routine part of resuscitation of premature neonates. Giving SAM at birth reduces the inflammatory response to mechanical ventilation and improves lung function.^[8]

At term, the fetal lung contains approximately 90 mL (30 mL/kg) of an ultrafiltrate of plasma. About 50 to 150 mL/kg/day of this fluid^[9] is produced by the lung and expelled into the mouth, where the fluid is swallowed or released into the amniotic fluid. Normally, there is no amniotic fluid in the lung. If the depth of fetal breathing

Figure 59-1 Intrathoracic pressures during delivery. Notice the increased intrathoracic pressure when the mouth and head have been delivered. (From Gregory GA: Resuscitation of the newborn. Anesthesiology 43:225, 1975.)

increases (e.g., during stress), as much as two thirds of the lung fluid volume (60 mL of amniotic fluid) is drawn into the lung and airways. Aspiration of amniotic fluid into the lung is indicated by the finding of squamous cells and other debris in the lungs of infants in whom gasping occurred in utero. Approximately two thirds of the normal amount of lung fluid is expelled from the lungs of a term neonate when the vagina and muscles of the pelvic floor squeeze the fetal chest during the birth process^[10] ( Fig. 59-1 ). The remaining fluid is removed by capillaries, lymphatics, and breathing. Small, preterm neonates; neonates born rapidly; and neonates born by cesarean section fail to get this "vaginal squeeze." As a result, these neonates have excess lung water at birth and may have more difficulty sustaining spontaneous respiration than neonates whose chests are squeezed effectively during the birth process. Retention of lung fluid results in transient tachypnea of the newborn. ^[11] Clearance of water from the lung is initiated by labor. Animals born by cesarean section after a period of labor have similar amounts of lung water as animals born vaginally. However, those born by cesarean section without previous labor have increased amounts of lung water.^[12] ^[13]

Neonates normally breathe by 30 seconds of age and sustain respiration by the time they are 90 seconds old. During birth, outward recoil of the compressed chest helps fill the lungs with air. For the first few breaths, the neonate expires less gas than he or she takes in, thereby establishing her or his functional residual capacity (FRC). Stimulation of the respiratory centers by mild acidosis, hypercarbia, hypoxia, pain, cold, touch, noise, and clamping of the umbilical cord initiates and sustains rhythmic respiration.^[14] ^[15] Severe acidosis, hypoxia, CNS damage, and maternal drugs (e.g., narcotics, barbiturates, local anesthetics, magnesium, alcohol) depress breathing. A few minutes after birth, the respiratory rate is 30 to 60 breaths/min. This rapid respiratory rate removes the increased carbon dioxide (CO₂ ) produced by the high oxygen consumption of the neonate (about 6 mL/kg/min) and helps maintain a normal FRC after it is established by not allowing sufficient time for the FRC to be expired.

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Figure 59-2 Diagram of the fetal circulation. The numbers within the circles are percentages of the combined ventricular output. (Adapted from Rudolph AM, Heymann MA: Fetal and neonatal circulation and respiration. Annu Rev Physiol 36:187, 1974.)

The circulation of the fetus is in parallel; that of the adult is in series^[16] ^[17] ( Fig. 59-2 ). The fetal right ventricle ejects two thirds of the combined ventricular output, and the left ventricle ejects one third.^[18] The disparity in output between the two ventricles of fetuses occurs because fetuses have both intracardiac and extracardiac shunts—the foramen ovale and ductus arteriosus. Blood returning from the placenta is well oxygenated. As a function of the anatomy, the inferior vena cava and foramen ovale direct oxygenated blood from the umbilical vein primarily to the left atrium. Poorly oxygenated blood from the superior vena cava is directed into the right ventricle and then into the pulmonary artery and ductus arteriosus. Ninety-five percent of the blood entering the pulmonary artery is shunted through the ductus arteriosus into the descending aorta.^[17]

The pulmonary vascular resistance (PVR), which is markedly elevated in utero, decreases dramatically in response to lung expansion, breathing, increased pH, and the increase in alveolar oxygen tension that occurs at birth.^[19] ^[20] PVR also decreases in the first 5 minutes to 24 hours of life because of recruitment and dilation of small arteries. During the next few weeks, PVR continues to decrease as the amount of arterial muscle is reduced. ^[21] Neonates born by cesarean section have higher pulmonary artery pressures and resistances than neonates delivered vaginally.^[22] Hypoxia, acidosis, hypovolemia, hypoventilation, atelectasis, and cold increase PVR.^[18] ^[23] The combination of hypoxia and acidosis increases PVR more than hypoxemia or acidosis alone.^[19]

The decrease in PVR at birth reduces pulmonary artery pressure and increases pulmonary blood flow. Systemic vascular resistance and left atrial pressure increase, preventing right-to-left shunting of blood through the ductus arteriosus. There often is left-to-right shunting of blood through the ductus arteriosus after birth. The increased pulmonary blood flow increases the volume of blood returning to the left atrium, which raises left atrial pressure above right atrial pressure and closes the foramen ovale. Closure of the foramen ovale prevents right-to-left shunting of blood through this structure. Anatomic closure of the foramen ovale may not occur for months, if ever. Consequently, if in the next few weeks to months right atrial pressure exceeds left atrial pressure (e.g., in cases of pneumonia, acidosis, or hypoxia), right-to-left shunting of blood will again occur through the foramen ovale.

The ductus arteriosus of animals born at term closes in response to oxygen, acetylcholine, parasympathetic nerve stimulation, and prostaglandins. ^[24] ^[25] ^[26] ^[27] ^[28] ^[29] A PaO₂ of 60 to 100 mm Hg constricts the ductus arteriosus of term lambs, but a PaO₂ of 300 to 500 mm Hg fails to constrict the ductus arteriosus of preterm animals. ^[27] Functionally, the ductus arteriosus closes when the pulmonary arterial pressure is less than systemic arterial pressure. Anatomically, the ductus arteriosus of term neonates may not close completely until the neonate is 10 to 14 days of age. It may take several months for the ductus arteriosus of preterm neonates to close. The parallel circulation of the fetus can be reestablished in term neonates if they become hypoxic, cold, or acidotic during the first 2 weeks of life. It can be reestablished in preterm neonates during the first several weeks of extrauterine life.