Although adrenergic receptors are thought to be mature at birth, sympathetic innervation is incomplete. After birth, neurotransmitter concentrations increase progressively, reflecting the maturation of sympathetic innervation. When compared to the adult, neonatal myocardium is more sensitive to norepinephrine.4 This phenomenon is a reflection of the relatively denervated status of neonatal myocardium. Dopamine is an indirectly acting inotrope that depends, in part, upon endogenous norepinephrine release for its action. Neonatal myocardium, being deficient in sympathetic innervation, is therefore less responsive to dopamine.
To meet the elevated metabolic demand, neonatal cardiac output, relative to body weight, is twice that of the adult. This is achieved with a relatively rapid heart rate (140 beats per minute) because as described earlier, stroke volume cannot be significantly increased. The neonatal circulation is characterized by centralization (increased peripheral vascular resistance and distribution of cardiac output primarily to vital organs), a situation comparable to an adult in compensated shock. Because neonatal baroreflex activity is impaired, the response to hemorrhage produces little increase in heart rate or change in total peripheral resistance. Thus, even a modest (10%) reduction in blood volume will cause a 15% to 30% decrease in mean blood pressure in the newborn infant. The structural and functional immaturity of the neonatal cardiovascular system severely limits the reserve that is available in the face of common perinatal and perioperative events such as hypovolemia, anesthetic-induced depression of contractility, relative bradycardia and positive pressure ventilation–induced decreases venous return. The marginal cardiovascular reserve of the neonate and leftward shift of the fetal hemoglobin dissociation curve are the rationale underlying the recommendation that the hematocrit be maintained at 30% or higher to prevent tissue ischemia in the newborn.
Respiratory Physiology of the Newborn
The respiratory system of a term neonate at birth is immature and postnatal development continues through early childhood. Although the conducting airways are fully developed by 16 weeks of gestation, the number of alveoli is reduced at birth. A premature infant born at 24 to 28 weeks of gestation is just beginning to develop alveoli from the distal saccules of the lung.5 Complete alveolar maturation does not occur until 8 to 10 years of age. Thus, the ratio of alveolar surface area to body surface area is one-third that of the adult. At birth, the infant possesses approximately one-tenth of the adult population of alveoli. To satisfy increased oxygen demand, neonatal alveolar minute ventilation is twice that of the adult. Increasing respiratory rate rather than tidal volume is the most efficient means to increase alveolar ventilation in the newborn. The diaphragm is the primary muscle of respiration in the neonate but has fewer high-oxidative muscle fibers and is thus less fatigue-resistant than in the adult. Ventilation-perfusion imbalance occurs as a result of distal airway closure during normal tidal breathing in the neonate. This phenomenon is responsible for an increase in the alveolar-arterial oxygen tension gradient compared to adults.
Adequate gas exchange depends on adequate alveolar recruitment and thus surfactant function. Production of surfactant begins by 23 to 24 weeks of gestation and reaches maturity at approximately 35 weeks of gestation. Surfactant-deficient preterm infants have decreased lung compliance and are at risk for the development of respiratory distress syndrome (RDS).5 Administration of corticosteroids to mothers in preterm labor may accelerate lung maturation in the fetus. Furthermore, the instillation of intratracheal exogenous surfactant in preterm babies has considerably improved the prognosis for premature infants. Infants born to mothers with intrauterine infection have a paradoxical increase in pulmonary maturation. The enhancement in lung maturation can be mimicked with lipopolysaccharide, suggesting that the effect is due to local inflammatory mediators rather than a downstream effect of corticosteroids.6 In humans, the effect of inflammation on lung maturation is not enhanced by corticosteroid administration.7
The neonatal chest wall is more compliant and has less outward recoil than that of the adult. Thus, the neonatal lung has a greater tendency to collapse and the infant is obliged to utilize active mechanisms to maintain normal lung volumes (Table 44-1). First, by breathing at a relatively rapid rate, the duration of expiration is limited. In this way, inspiration is initiated before the lung has completed recoiling to its end-expiratory volume. Second, the neonate utilizes intercostal muscle activity during expiration to stabilize the chest wall, thus retarding the decline in lung volume during expiration. Last, the neonate exhales through a partially closed glottis, also retarding expiratory flow and maintaining end-expiratory lung volume. The awake neonate has a functional residual capacity (FRC) that is similar, when normalized to body weight, to that of an adult. However, because neonatal alveolar ventilation is twice that of an adult, the ratio of alveolar ventilation to FRC in the neonate is twice that of the adult. The high ratio of minute ventilation to FRC causes a much more rapid wash-out or wash-in of oxygen and anesthetic drugs in response to changes in inspired concentrations.
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