The cardiovascular system undergoes several changes during the transition to extrauterine life. Closure of the ductus venosus and foramen ovale converts the circulatory system from a parallel circuit to a series circuit. Hypoxia, hypercarbia, sepsis, and hypothermia can cause undesirable right-to-left shunting of blood through the foramen ovale and ductus arteriosus, the anatomic closure of which may not be complete until 2 weeks after birth. Pulmonary vascular resistance, elevated during fetal life and immediately after birth, decreases rapidly at first and attains adult values by 2 months of age. During this time, however, the pulmonary vascular resistance is labile, and considerable constriction and dilation can result from physiologic, pharmacologic, and environmental manipulations. The syndrome of persistent pulmonary hypertension of the newborn—characterized by refractory hypoxemia, hypercarbia, and acidosis—is common in patients with diaphragmatic hernias but can occur in virtually any stressed term infant.

Because it must work against increased resistance in utero, the right ventricle is hypertrophied and dominant in the newborn. Both the left and right ventricles are noncompliant and myocardial tissue of the newborn has 30% fewer contractile elements than that of the adult.⁸⁹

Increases in preload cannot increase stroke volume because of the diminished contractility of the newborn myocardium.⁸¹ The infant is functioning on an unfavorable portion of Starling’s curve; only a modest increase in filling pressure can precipitate congestive heart failure. Therefore the anesthesiologist must scrupulously avoid overzealous administration of intravenous fluids.

The cardiac output of a newborn (180–240 mL/kg per minute) is two to three times the adult value relative to size. This difference reflects the greater oxygen consumption and metabolic rate in this age group. Increases in cardiac output are achieved primarily by increases in heart rate (normal, 120–160 bpm), because the infant’s myocardial contractility is relatively fixed. Sympathetic innervation of the heart is incomplete, further impairing the ability to increase stroke volume.⁹⁴ Systemic blood pressure is low in the newborn period (Table 24-1).⁷⁷ Furthermore, infants with birth asphyxia and those on ventilators have lower blood pressures.⁴⁰ Awareness of normal values is essential for the appropriate diagnosis and treatment of hypotension.

The trachea has an incompletely developed cartilaginous framework. Any extrathoracic obstruction, such as postextubation mucosal edema, can cause tracheal collapse distally. Even a 1-mm ring of tracheal narrowing can cause severe respiratory distress because of the already small airway caliber (Fig. 24-1). The infant has a highly compliant chest wall because of a horizontally oriented rib cage.⁶³ In diseases of poor lung compliance (e.g., pulmonary edema and atelectasis), excessive lung recoil results in greater retraction of the soft chest wall and more loss of functional residual capacity than would occur in older children with stiffer chest walls.

When the newborn is supine, its closing capacity impinges on normal tidal breathing. As a result, small airway collapse leads to atelectasis, ventilation/perfusion mismatch, and hypoxia.⁷³ The anesthesiologist can use controlled ventilation and positive end-expiratory pressure (PEEP) to help prevent this situation.

Because of their high oxygen consumption and increased work of breathing, infants breathe at rapid rates of 30 to 50 bpm. The diaphragm of an infant has a preponderance of fast-twitch muscle fibers, which are prone to early fatigue.¹⁹ Conditions causing increased work of breathing are therefore not tolerated for long periods of time and may result in hypercarbia and respiratory failure.

Chemical and neural control of breathing is different in the newborn. The response to hypoxia is paradoxic, characterized by a brief period of hyperpnea, followed by apnea.⁷⁰ The central
chemoreceptors have a diminished sensitivity to PCO₂ compared with those of adults, that is, a higher PCO₂ is needed to effect a similar increase in minute ventilation. Periodic breathing and apneic spells are common in the newborn, making close monitoring of respiratory function mandatory in the postoperative period.^68,69

Oxygen unloading at the tissue level is made more difficult by the high percentage of fetal hemoglobin in newborn erythrocytes. Because of its lower P₅₀, hemoglobin F “holds on” to oxygen more tenaciously than does adult hemoglobin. The generally high hemoglobin concentration at birth (15–18 g/dL) is beneficial in increasing oxygen delivery to the cells.

Maintenance of normothermia is essential in the newborn. Adverse effects of hypothermia include apnea, hypoglycemia, metabolic acidosis, and increased oxygen consumption. Because of decreased subcutaneous tissue, a low surface area-to-volume ratio, and small body mass, the neonate has increased environmental heat losses. Nonshivering thermogenesis, mediated by catecholamine effects on brown fat deposits, is the primary heat-generating process in the newborn. This process increases oxygen consumption by as much as 200-fold. Methods of preventing heat loss intraoperatively include increasing ambient temperature and using radiant warmers, heating blankets, intravenous fluid warmers, and humidified anesthetic gases.¹² Covering the top of the head and extremities with plastic wrap effectively minimizes evaporative heat losses during surgical procedures.⁶ Moreover, the use of forced-air warming covers and passive heat- and moisture-exchanging filters has significantly diminished heat loss in pediatric surgical patients.^13,53

Hypoglycemia occurs frequently in this age group, especially in the premature infant, the small-for-gestational-age infant, and the infant of a diabetic mother. Causative factors in the development of neonatal hypoglycemia include diminished hepatic glycogen stores, decreased gluconeogenetic capabilities, and decreased response to glucagon secretion.⁷⁴ Blood glucose values should be monitored frequently and adjusted using dextrose containing fluids accordingly. Normal blood glucose values in the newborn are listed in Table 24-2.⁷⁵

Inhalation anesthetic agents are commonly administered with O₂ and air during maintenance of anesthesia. Anesthetics such as nitrous oxide, sevoflurane, desflurane, and isoflurane have been used in pediatric thoracic surgical patients. Sevoflurane
has many advantages in the pediatric patient owing to the combination of rapid onset and nonpungency, making this agent ideal for inhalation induction.⁵⁴ Isoflurane may be preferred for thoracic surgery since it exhibits less attenuation of HPV compared with other inhalation agents. All volatile agents cause a dose-dependent depression of cardiac function in addition to impaired baroreceptor reflexes.^18,84 Hypotension and bradycardia commonly occur when potent inhalation agents are administered in high concentrations. Because all potent inhaled anesthetics have a low therapeutic index in infants, they must be used sparingly, with close attention to blood pressure and heart rate. Nitrous oxide can increase pulmonary vascular resistance, which is undesirable in neonates, with their potential for persistent pulmonary hypertension.²⁶ Clinical studies have shown, however, that nitrous oxide can be used in infants without a significant increase in right-to-left shunting.⁴¹