Anatomy and Physiology

Upper airway
1. Neonates are obligate nose breathers due to weak oropharyngeal muscles and increased compliance of the pharynx, larynx, and bronchial tree. Their nares are relatively narrow, and a significant fraction of the work of breathing is needed to overcome nasal resistance. Occlusion of the nares by bilateral choanal atresia or tenacious secretions can cause complete airway obstruction; however, some infants will convert to mouth breathing. Placement of an oral airway, a laryngeal mask airway, or an endotracheal tube may be necessary to reestablish airway patency during sedation or anesthesia.
2. Infants have relatively large tongues, which can make mask ventilation and laryngoscopy challenging. A recent study called tongue size into question and found the tongue to be proportional in children aged 1 to 12. Clinically, the tongue can easily obstruct the airway if excessive submandibular pressure is applied during mask ventilation.
3. Infants and children have a more cephalad glottis (C3 vertebral level in premature infants, C4 in infants, and C5 in adults) and a narrow, long, angulated epiglottis, which can make laryngoscopy difficult.
4. In infants and young children, the narrowest part of the airway is at the cricoid cartilage (recent studies have questioned this; see suggested readings), rather than at the glottis (as in adults). An endotracheal tube that passes through the cords may still be too large distally.
5. Deciduous teeth erupt within the first year and are shed between ages 6 and 13 years. To avoid dislodging a loose tooth, it is safest to open the mandible directly, without introducing a finger or appliance into the oral cavity. Loose teeth should be documented on the preoperative evaluation. In some instances, unstable teeth should be removed before laryngoscopy. Parents and patients should be informed of this possibility in advance.
6. Airway resistance in infants and children can be increased dramatically by subtle changes in an already small-caliber system. Even a small amount of edema can significantly increase airway resistance and cause airway compromise.
Pulmonary system
1. Neonates have higher metabolic rates, resulting in an elevated oxygen consumption (6 mL/kg/min) when compared with adults (3 mL/kg/min).
2. Neonatal lungs have high closing volumes, which fall within the lower range of their normal tidal volume. Below closing volume, alveolar collapse and shunting occur.
3. To meet the higher oxygen demand, infants have a higher respiratory rate and minute ventilation. An infant’s functional residual capacity (FRC) is nearly equivalent to that of an adult (FRC of an infant, 25 mL/kg; adult, 35 mL/kg). Their higher minute ventilation to FRC ratio results in rapid inhalational induction. The tidal volume for infants and adults is equivalent (6-7 mL/kg).
4. Anatomic shunts including PDA and patent foramen ovale may develop significant right-to-left flow with increases in pulmonary artery pressure (eg, hypoxia, acidosis, or high positive airway pressure). This may predispose to air emboli if care is not taken to remove it from the IV tubing.
5. The characteristics of the infant’s pulmonary system contribute to rapid desaturation during apnea. Profound desaturation can occur when an infant coughs or strains and alveoli collapse. Treatment may require deepening anesthesia, using neuromuscular relaxants, as well as alveolar recruitment.
6. The diaphragm is the infant’s major muscle of ventilation. Compared with the adult diaphragm, the newborn has only half the number of type I, slow-twitch, high-oxidative muscle fibers essential for sustained increased respiratory effort. Thus, the infant’s diaphragm fatigues earlier than the adult’s. By 2 years of age, the child’s diaphragm would have attained mature levels of type I fibers.
7. The pliable rib cage (compliant chest wall) of an infant cannot maintain negative intrathoracic pressure easily. This diminishes the efficacy of the infant’s attempts to increase ventilation.
8. An infant’s dead space is 2 to 2.5 mL/kg, equivalent to an adult’s.
9. Infants’ high baseline minute ventilation limits their ability to increase their ventilatory effort further. End-tidal CO₂ concentrations should be followed if spontaneous ventilation is permitted under anesthesia; assisted or controlled ventilation may be necessary.
10. Alveolar maturation occurs by 8 to 10 years of age when alveoli number and size reach adult ranges.
11. Retinopathy of prematurity (see Chapter 30).
12. Apnea and bradycardia after general anesthesia occur with increased frequency in infants who are premature and in infants who have anemia, sepsis, hypothermia, central nervous system disease, hypoglycemia, hypothermia, or other metabolic derangements. These patients should have cardiorespiratory monitoring for a minimum of 24 hours postoperatively. Such infants are not candidates for ambulatory day surgery. The guidelines for discharge vary among institutions. Most hospitals agree that infants who are less than 45 to 60 weeks of postconceptual age are monitored postoperatively. Any full-term infant who displays apnea after general anesthesia should also be monitored.

Cardiovascular system

Heart rate and blood pressure vary with age and should be maintained at age-appropriate levels perioperatively (Tables 33.3 and 33.4).

Table 33-3 Age Dependence of Typical Respiratory Parameters

Variable	Newborn	1 Y	3 Y	5 Y	Adult
Respirations (breaths/min)	40-60	20-30	Gradual decrease to 18-25	18-25	12-20
Tidal volume (mL)	15	80	110	250	500
FRC (mL/kg)	25		35		40
Minute ventilation (L/min)	1	1.8	2.5	5.5	6.5
Hemoglobin (g/dL)	14-20	10-11	–	–	13-17
Hematocrit (%)	47-60	33-42			38-50
Arterial pH	7.30-7.40	7.35-7.45	–	–	–
PaCO₂ (mm Hg)	30-35	30-40	–	–	–
PaO₂ (mm Hg)	60-90	80-100	–	–	–

FRC, functional residual capacity.

Table 33-4 Cardiovascular Variables

Age	Blood Pressure (mm Hg)
Age	Heart Rate (Beats/min)	Systolic	Diastolic
Preterm neonate	120-180	45-60	30
Term neonate	100-180	55-70	40
1 y	100-140	70-100	60
3 y	84-115	75-110	70
5 y	84-100	80-120	70

Cardiac output is 180 to 240 mL/kg/min in newborns, which is two to three times that of adults. This higher cardiac output is necessary to meet the higher metabolic oxygen consumption demands.
The ventricles are less compliant and have a relatively smaller contractile muscle mass in newborns and infants. The ability to increase contractility is limited; increases in cardiac output occur by increasing heart rate rather than stroke volume. Bradycardia is the most deleterious dysrhythmia in infants, and hypoxemia is a frequent cause of bradycardia in infants and children.
Neonates have immature calcium signaling and handling in the scarcoplasmic reticulum and myocardium and are more dependent on ionized calcium concentrations for myocardial function.

Fluid and electrolyte balance
1. The glomerular filtration rate at birth is 15% to 30% of the normal adult value. Adult value is reached by 1 year of age. Renal clearance of drugs and their metabolites is diminished during the first year of life.
2. Neonates have an intact renin-angiotensin-aldosterone pathway, but the distal tubules resorb less sodium in response to aldosterone. Thus, newborns are “obligate sodium losers,” and IV fluids should contain sodium.
3. The total body water in the preterm infant is 90% of body weight. In term infants, it is 80%; at 6 to 12 months, it is 60%. This increased percentage of total body water affects drug volumes of distribution. The dosages of some drugs (eg, propofol, succinylcholine, pancuronium, and rocuronium) are 20% to 30% greater than are the equally effective dose for adults.
Hematologic system
1. Normal values for hemoglobin and hematocrit are listed in Table 33.3. The nadir of physiologic anemia is at 3 months of age, and the hemoglobin may reach 10 to 11 g/dL in an otherwise healthy infant. Premature infants may demonstrate a decrease in hemoglobin concentration as early as 4 to 6 weeks of age.
2. At birth, fetal hemoglobin (HbF) predominates, but β-chain synthesis shifts to the adult type (HbA) by 3 to 4 months of age. HbF has a higher affinity for oxygen; that is, the oxyhemoglobin dissociation curve is shifted to the left, but debate exists regarding the clinical relevance.
3. See Section XII.B for calculations of blood volume and red cell mass.
Hepatobiliary system
1. Liver enzyme systems, particularly those involved in phase-II (conjugation) reactions, are immature in the infant. Drugs metabolized by the P-450 system may have prolonged elimination times.
2. Jaundice is common in neonates and can be physiologic or have pathologic causes.
3. Hyperbilirubinemia and displacement of bilirubin from albumin by drugs can result in kernicterus. Premature infants develop kernicterus at lower levels of bilirubin than do term infants.
4. Plasma levels of albumin are lower at birth and as a result, drugs that are protein bound may have a higher free fraction and higher effective concentration.
Endocrine system
1. Newborns, particularly premature babies and SGA infants, have decreased glycogen stores and are more susceptible to hypoglycemia. Infants of diabetic mothers have high insulin levels because of prolonged exposure to elevated maternal serum glucose levels and are prone to hypoglycemia. Infants who fall into these groups may have dextrose requirements as high as 5 to 15 mg/kg/min. Normal glucose concentrations in the full-term infant are ≥45 mg/dL (2.5 mmol/L).
2. Hypocalcemia is common in infants who are premature, are SGA infants, have a history of asphyxia, are offspring of diabetic mothers, or have received transfusions with citrated blood or fresh-frozen plasma. Serum calcium concentration should be monitored in these patients and calcium administered if the ionized calcium is less than 4.0 mg/dL (1.0 mmol/L).
Temperature regulation
1. Compared with adults, infants and children have a greater surface area to body weight ratio, which increases loss of body heat.
2. Infants have significantly less muscle mass and cannot compensate for cold by shivering or adjusting their behavior to avoid the cold.
3. Infants respond to cold stress by increasing norepinephrine production, which enhances metabolism in brown fat. Norepinephrine also produces pulmonary and peripheral vasoconstriction, which can lead to right-to-left shunting, hypoxemia, and metabolic acidosis. Sick and preterm infants have limited stores of brown fat and therefore are more susceptible to cold. Strategies to prevent cold stress are discussed in Section IV.C.

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