They have a large head and large tongue with a short neck.

The tongue is relatively large.

Neonates are obligate/preferential nasal breathers (till 5 months of age).

The larynx is high (C3–C4) and anterior. The epiglottis is long, floppy, and U-shaped. It tends to fall posteriorly in the supine position. Unlike the “sniffing” position, the head needs to be in a neutral position to improve the glottic view.

The airway is funnel-shaped with the narrowest part at the level of the cricoid cartilage.

The trachea is short (4–5 cm in the neonate). There is a high chance of endotracheal tube (ETT) dislodgement or endobronchial migration of ETT with head movement.

Limited respiratory reserve, absent “bucket handle” action of ribs, diaphragmatic breath­ing, and low functional residual capacity (FRC) due to highly compliant chest wall.

FRC further decreases with apnea and anesthesia, causing lung collapse.

The closing volume is larger than the FRC until 6 to 8 years of age. This causes an increased tendency for airway closure at end-expiration. Thus, neonates and infants generally need positive pressure ventilation (PPV) with positive end-expiratory pressure (PEEP) during anesthesia.

The diaphragm has a lower percentage of type I muscle fibers and therefore easily subject to fatigue.

The development of alveoli occurs over the first 8 years of life.

Premature infants are at risk of apneas in the postoperative period.

Respiratory distress syndrome (RDS) is frequent at <28 weeks due to reduced surfactant.

Patent ductus arteriosus (PDA) more common in premature infants; it closes typically 10 days to 2 weeks after birth but may reopen in the first few weeks after birth whenever pulmonary arterial pres­sure rises (hypoxemia, hypercarbia, aci­dosis, etc.), which is known as transitional circulation.

The neonatal heart is poorly compliant and has reduced contractile force due to dis­organized intracellular contractile proteins and immature sarcoplasmic reticulum.

The cardiac output is rate-dependent in neonates and children with reduced capacity to increase stroke volume by premature heart. Therefore, bradycardia is poorly tolerated, and cardiac compression should be provided in the neonate with a heart rate < 60 bpm.

The dominant vagal tone makes neonates and infants prone to bradycardia.

The glomerular function and tubular fun­ction mature by 2 years and 8 months of life, respectively.

Normal urine output ranges between 1 and 2 mL/kg/h.

Liver cytochrome P-450 enzymes achieve maturity at the adult level by 6 months.

Premature infants are prone to hypo­glycemia because of hepatic glycogen storage development in the last few weeks of gestation.

The hemoglobin is around 18 to 20 g/dL at the time of birth, which decreases to 9 to 12 g/dL over the next 3 to 6 months.

At birth, HbF is the predominant hemo­globin (70–80%), the levels of which drop to around 5% within 3 months.

The deficiency of vitamin K-dependent clotting factors and platelets during the first few months of life puts neonates at risk of intracranial bleed. Therefore, vitamin K is given at birth to prevent hemorrhagic disease of the newborn.

Neonates and preterms are more prone to heat loss due to:

• Relatively larger body surface-to-body weight ratio.

• Poorly developed subcutaneous tissue.

• Inability to use shivering thermogenesis.

These are partially compensated for by nonshivering thermogenesis via brown fat, which is inhibited by volatile and intravenous anesthetics.

Hypothermia leads to cardiovascular stress, delays emergence from anesthesia.