In utero, the high pulmonary vascular resistance allows for a parallel circulation, whereby both ventricles pump systemically with less than 10 % of the cardiac output entering the pulmonary system. To allow adequate placental oxygenated blood flow to the fetus, there are three shunts in utero: the ductus venosus, the foramen ovale, and the ductus arteriosus (Fig. 39.1). Oxygenated placental blood preferentially shunts across the foramen ovale because of relatively high right-sided heart pressures in utero (right to left shunt).

At birth, the pulmonary vascular resistance drops with the expansion of both lungs, thus promoting pulmonary blood flow and elevating the PO₂. As the left atrial pressure rises above right atrial pressure, the foramen ovale functionally closes; however, it still remains open in approximately 20 % of neonates. Upon exposure to higher PO₂, the ductus venosus almost immediately closes, while the ductus arteriosus musculature constricts leading to closure in a majority of term neonates (may remain open in some premature neonates).

The neonatal ventricle is rather noncompliant with a steep pressure-volume relationship that resembles the elderly population (fixed stroke volume). Therefore, inadequate preload leads to a stiff underfilled ventricle and hence low systemic pressures. Although hypotension after anesthetic induction usually responds to volume administration, practitioners must avoid overloading these patients. Volume overload can lead to pulmonary edema because the left ventricular myofibrils have decreased contractile mass. Moreover, the sarcoplasm sequesters Ca²⁺ (ineffective Ca²⁺ adenosine triphosphatase activity), thus impairing myocardial contractility. In addition, the neonatal ventricle tolerates afterload poorly because of relative noncompliance and poor contractility.

The underdeveloped neonatal sympathetic nervous system leads to a predominance of parasympathetic tone, and hence neonates are more prone to bradycardia under hypoxic conditions. Cardiac output in neonates/infants is heart rate “dependent” because of the fixed stroke volume. With a resting heart rate of 120–160 bpm (Table 39.2), bradycardia (<80 bpm) significantly impacts the cardiac output.

Circulating blood volume is highest for premature neonates (100 ml/kg), 85 ml/kg for term neonates, as compared with adults (70 ml/kg). Neonates have a hematocrit of about 60 %. The nadir in hematocrit occurs at about 6 months leading to a hemoglobin of 9 g/dl (hematocrit of 27 %). Because healthy neonates tolerate anemia better, blood transfusions may be deferred until the hemoglobin reaches 6–7 g/dl. However, the presence of congenital cyanotic heart disease or severe pulmonary disease has a higher trigger (Hb 10–13 g/dl) for blood transfusion. All neonates should receive irradiated blood to prevent graft-versus-host disease (where the donor lymphocytes attack the recipient’s bone marrow). Lastly, the platelet count should be greater than 50,000/mm³ to ensure the formation of an adequate primary hemostatic plug.

At birth, the GFR is 15–30 % of adult values (20–40 ml/min/1.73 m² compared to 120 ml/min/1.73 m²) because of reduced nephron function, high renal vascular resistance, and low systemic perfusion pressures. In the 1st month, urine output is 1–2 ml/kg/h, but reduced GFR means large-volume administration can lead to hypervolemia and volume overload. Renally excreted drugs have a prolonged effect until the GFR approaches adult values at the end of 1 year. Because of decreased renal tubular function, neonates poorly concentrate urine as the medullary countercurrent exchange systems are immature. Both retention and excretion of sodium are impaired in neonates.

Neonates have proportionately a higher percentage of total body water (TBW) per kg body weight than adults, with fetuses having TBW of 90 %, preterm neonate 80 %, and full-term neonate 70 % of body weight. By 1 year, TBW decreases to the adult value of 60 % body weight. Initially, neonates have a predominance of extracellular fluid (ECF), which mobilizes as the GFR increases. Maintenance fluid requirements in neonates follow similar adult formulas; however, maintenance fluid should include sodium because of the reduced distal tubular reabsorption of sodium.

Neonates and young infants have a large surface area to body weight ratio causing rapid heat loss in the operating room. The primary mechanisms for neonatal heat loss are conduction and radiation, with convection and evaporation playing a less significant role. Because neonates do not shiver, heat production occurs through non-shivering thermogenesis due to brown fat metabolism. Neonatal oxygen consumption is already elevated compared to adults (6 ml/kg/min vs. 3 ml/kg/min), and increased oxygen consumption due to cold stress may produce metabolic acidosis, cardiac irritability, or respiratory depression in compromised neonates. Heat loss can be prevented by using forced air-warming device, warm blankets, and warm intravenous fluids and most importantly by increasing the operating room temperature to 26 °C or higher. Heat lamp radiation is beneficial; however, it may produce mild burns when used too close to the skin.

As compared to adults, the normal pediatric airway has a cephalad glottis (C4 vs. C6 in adults), large tongue, prominent occiput, long epiglottis, and short trachea and neck, with the narrowest part of the pediatric airway being the cricoid ring. Because neonates and infants <6 months are preferentially nasal breathers, bilateral choanal atresia can lead to complete airway obstruction. Airway management in healthy children is usually straightforward; however, airway management in craniofacial syndromes, such as Pierre Robin syndrome (micrognathia, retrognathia, and glossoptosis—large tongue in relation to oropharynx) or Treacher Collins syndrome (mandibular facial dysostosis with severe hypoplasia of the mandible and zygomatic arches), can be challenging.

Neonates born of gestational age <37 weeks are labeled as preterm neonates. Preterm neonates have some unique differences than full-term neonates. Aberrant retinal vascular development leads to retinal tears and detachment and ultimately blindness, termed as retinopathy of prematurity (ROP). Risk factors for ROP include prematurity, low birth weight, and exposure to supplemental oxygen. Therefore, supplemental oxygen should be avoided, whenever possible, in neonates until 44 weeks of postgestational age and if given, should have a goal of maintaining oxygen saturation in the low 90 %.

Premature neonates are prone to the development of respiratory distress syndrome as the lungs mature after 34 weeks of gestation. Surfactant production begins at 26 weeks of gestation and enough is produced at 34 weeks of gestation for the alveoli to remain open. Neonates requiring supplemental oxygen at 36 weeks of gestation are said to have chronic lung disease. Premature neonates, because of reduced hepatobiliary function, are prone to hypoglycemia and hypocalcemia. Often they require dextrose-containing solutions for maintenance.

Preterm neonates are susceptible to apnea and thus require continous pulse oximetry monitoring in the post-operative period. Preterm neonates may have a hematocrit of 40 % as compared to 60 % for full term neonates, and this anemia further increases the risk of apnea. This predisposes a preterm infant to apnea. Moreover, preterm infants often have vitamin K deficiency and thrombocytopenia. Therefore, elective surgery should be deferred until 60 weeks postgestational age in preterm neonates. If surgery is performed before 60 weeks postgestational age, then these neonates are admitted postoperatively for observation for apneic episodes.