Circulation

After delivery, the neonatal circulation undergoes numerous changes as it transitions from fetal circulation to adult-type circulation over the first days to weeks of life ( Table 64-1 ). Pulmonary vascular resistance (PVR) decreases rapidly on the first day of life, and pulmonary blood flow increases. Pressure on the left side of the heart increases with an increase in pulmonary venous return and systemic vascular resistance. These changes, along with higher oxygen levels, promote functional closure of two in utero connections between the right and left sides of the circulation. Mechanical closure continues over weeks to months. During this transitional period, the circulation can alternate between fetal and adult because shunts can reopen under certain conditions. Close attention must be paid to changes in hemodynamics during anesthesia and surgical stress because they can induce circulatory changes that can trigger shunt reopening. Numerous factors can increase the risk of prolonged transitional circulation, including prematurity, elevated PVR, acidosis, hypothermia, meconium aspiration, and congenital heart disease (CHD).

Cardiovascular

Myocardium in infants is stiff and poorly compliant secondary to poorly developed contractile cellular mass compared with older children. Stroke volume is relatively fixed making the increased cardiac output predominately rate dependent. Because the infant heart normally functions at the top of the Frank-Starling curve, changes in volume or afterload are poorly tolerated. Preoperative fasting and other perioperative fluid deficits must be accounted for.

The neonate has a poorly developed sympathetic nervous system, which is unable to compensate for periods of stress with changes in heart rate, preload, or afterload. Infants are considered “vagotonic” because of the imbalance between the immature sympathetic and developed parasympathetic systems. Infants often respond initially with bradycardia when they become hypoxic or stimulated, such as during laryngoscopy. Neonatal sarcoplasmic reticulum has reduced calcium storage ability, making the heart susceptible to cardiac depression from changes in calcium levels or from the depressant effects of anesthetic agents .

Pulmonary

Lung development continues in utero much later than other organs. The lungs cannot function on their own ex utero until 34–36 week gestational age, when lung volume, surface area for gas exchange, and surfactant production to help keep small airways open all have developed adequately. Alveolar maturation continues postnatally, increasing in size and number, for approximately 8 years. The relatively small number and size of neonatal alveoli lead to reduced lung compliance and small airways prone to closure. In contrast, the cartilaginous neonatal rib cage makes the chest wall highly compliant. As a result, the ribs provide less support to maintain open alveoli. The work of breathing is increased with the subsequent breath to reexpand these closed airways. These factors cause a higher closing volume, with small airway closure during normal tidal volume.

Minute ventilation (or alveolar ventilation) is higher than in adults secondary to an increased respiratory rate because tidal volume on a per kilogram basis is the same as in adults. The alveolar ventilation-to-functional residual capacity ratio is higher because of the increased alveolar ventilation (5:1 vs. 1.5:1 in adults). Additionally, oxygen consumption is increased twofold to threefold. These factors, limited oxygen stores and increased oxygen demand, lead to rapid oxyhemoglobin desaturation during periods of apnea or airway obstruction.

The diaphragm and intercostal muscles are composed of two types of muscle fibers. Type I fibers are fatigue-resistant, and type II fibers are fatigue-prone and less energy efficient. The neonate has a decreased amount of type I fibers, resulting in an increased work of breathing and early fatigue if airway obstruction occurs. Under general anesthesia, there is a further increase in chest wall compliance because of muscle relaxation. At end expiration, the lungs reach a lower volume. Consequently, it takes more work to open airways during the next breath. For this reason, tracheal intubation is indicated during general anesthesia.

The respiratory drive to hypoxia or hypercarbia is not yet developed. Both stimuli induce respiratory depression and breath holding.

Pediatric airway

The neonatal airway has numerous anatomic differences that must be accounted for. Infants have a proportionally larger head and tongue with a shorter trachea and neck than adults. The large tongue may make mask ventilation difficult and necessitate use of an oral airway to relieve airway obstruction. The neonate’s upper airway is susceptible to closure, especially if the head is flexed when lying supine owing to the relatively large occiput. Use of a shoulder roll may help open the airway and improve visualization of the glottic region. The larynx is located more cephalad (C4 vs. adult level of C5) with an epiglottis that is short, omega-shaped, and angled over the glottic opening. The larynx in a preterm infant is even more cephalad, located at the C3 level. These differences make straight laryngoscope blades especially useful in the neonatal period. The narrowest portion of the airway is the cricoid cartilage, necessitating performance of a leak test around a cuffed or uncuffed endotracheal tube, with an ideal leak <30 cm H ₂ O but greater than peak airway pressures. The anterior attachment of the vocal cords in infants is more caudad than the posterior attachment, in contrast to the adult vocal cords that are perpendicular to the tracheal axis. When placing the tracheal tube, it often becomes hung up at the anterior commissure. This situation is particularly problematic when performing nasal intubations. When placing the tracheal tube, every effort should be made to introduce it through the posterior aspect of the vocal cords.

Kidneys

Glomerular filtration rate (GFR) and tubular function reach maturation around 5 months of age, although this is delayed in premature infants. GFR is approximately 40% of adult values in neonates and even lower in preterm infants, with GFR values proportional to gestational age. This decreased GFR results in decreased creatinine clearance; immature diluting and concentrating ability; and impaired sodium, glucose, and bicarbonate management in neonates. These problems are worse in preterm infants. Decreased GFR impairs excretion of saline, excessive water, and medications. Renal function approaches adult values around 2 years of age.

Liver

The liver builds up its glycogen stores primarily in the last trimester of fetal life; this means preterm infants have missed much and ELGANs have missed nearly all of their intrauterine glycogen storage time. Although term infants are susceptible to hypoglycemia, this is especially a concern in preterm neonates. Glucose hemostasis management is imperative in the perioperative setting. Maintenance glucose requirement for preterm infants is 8–10 mg/kg per minute, whereas in full-term neonates it is 5–8 mg/kg per minute.

The liver is the primary site for drug metabolism, which is slower in neonates, owing in part to relatively lower hepatic blood flow. Decreased metabolism in this population is secondary to deficiencies of many of the enzymes required for oxidation, reduction, hydrolysis, and conjugation of medications. Many enzymes still need to be exposed to toxins or drugs, which serve to stimulate and induce further development of these enzymatic pathways.

Gastrointestinal

There is an increased incidence of gastroesophageal reflux in infants until age 4–5 months, with the rate particularly high in preterm infants, secondary to decreased lower esophageal sphincter tone.

Thermoregulation

Heat loss to the environment is particularly high in the neonatal period because of thin skin, poor fat stores, and a high surface-to-weight ratio. Fully developed epidermis is present only after 32 weeks gestational age, making preterm newborn skin a large source of heat and water loss. Evaporative loss of water can be 5–6 mL/kg per hour. Cold is poorly tolerated because it increases oxygen consumption and leads to metabolic acidosis. In contrast to adults, neonates are unable to preserve or generate heat by peripheral vasoconstriction and shivering. Neonates produce heat by nonshivering thermogenesis that occurs predominately in brown fat that is rich in mitochondria. Brown fat is located between the scapulae, in the axillae and mediastinum, and around the adrenal glands. Increased sympathetic output results in an increase in circulating norepinephrine and thyroid-stimulating hormone that uncouples oxidative phosphorylation in brown fat, generating heat. Approximately 25% of the cardiac output is diverted to brown fat resulting in direct warming of the blood. This process uses vital energy stores in neonates and takes a high caloric toll. Circulating norepinephrine increases PVR. Neonates left exposed to room air can lose 150 kcal per minute. Anesthetic agents negatively affect nonshivering thermogenesis.

Hematologic development

In utero, the predominant hemoglobin is fetal hemoglobin (HbF), which is characterized by high affinity for oxygen. HbF is 50% saturated with oxygen (P ₅₀ ) at 19 mm Hg. The P ₅₀ of adult hemoglobin (HbA) is 27 mm Hg. In utero, HbF efficiently delivers oxygen to the relatively hypoxic tissues. However, ex utero, when tissue oxygen levels increase, HbF delivers oxygen less efficiently than HbA. Transfusion thresholds are higher in infants who have predominantly HbF compared with infants whose hemoglobin has converted to HbA. A preterm infant who received blood transfusions in the NICU would have predominantly HbA depending on the total amount transfused. Transfusion thresholds should be considered based on the HbA profile.

Normal hemoglobin values at birth are as follows:

Full-term newborn	14–20 g/dL
Preterm newborn, 32–36 weeks gestational age	13–14 g/dL
Preterm newborn, 28–32 weeks gestational age	12–13 g/dL

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