The editors would like to acknowledge that this chapter is abridged from a chapter originally written by Dr. Seamas Dore.
ANATOMIC & PHYSIOLOGICAL DEVELOPMENT
Compared with older children and adults, neonates and infants have weaker intercostal muscles and weaker diaphragms (due to a paucity of type I fibers). Consequently, they have less efficient ventilation, more pliable and coursing ribs, and protuberant abdomens. Alveoli are fully mature by about 8 years of age. The respiratory rate is increased in neonates and gradually falls to adult values by adolescence. Tidal volume and dead space per kilogram are nearly constant during development. Neonates and infants have fewer and smaller alveoli, reducing lung compliance; in contrast, their cartilaginous rib cage makes their chest wall very compliant and increases airway resistance. Work of breathing is increased, and respiratory muscles fatigue more easily. These characteristics promote chest wall collapse during inspiration and relatively low residual lung volumes at expiration. The resulting decrease in functional residual capacity (FRC) limits oxygen reserves during periods of apnea (eg, intubation attempts) and predisposes neonates and infants to atelectasis and hypoxemia. These effects of reduced FRC may be exaggerated by the relatively higher rate of oxygen consumption of neonates and infants, 6–8 mL/kg/min versus 3–4 mL/kg/min in adults. Moreover, hypoxic and hypercapnic ventilatory drives are not fully developed in neonates and infants. In contrast to adults, hypoxia and hypercapnia may depress respiration in these patients.
Neonates and infants have, compared with older children and adults, a proportionately larger head and tongue, narrower nasal passages, an anterior and cephalad larynx (the glottis is at a vertebral level of C4 versus C6 in adults), a longer epiglottis, and a shorter trachea and neck. These anatomic features make neonates and young infants obligate nasal breathers until about 5 months of age. The cricoid cartilage is the narrowest point of the airway in children younger than 5 years of age; in adults, the narrowest point is the glottis (vocal cords).
Cardiac stroke volume is relatively fixed by the immature, noncompliant left ventricle in neonates and infants. The cardiac output is therefore very sensitive to changes in heart rate. Although basal heart rate is greater in neonates and infants than in adults (Table 30–1), vagal stimulation, anesthetic overdose, or hypoxia can quickly trigger bradycardia with profound reductions in cardiac output. Sick infants undergoing emergency or prolonged surgery appear particularly prone to episodes of bradycardia that can lead to hypotension, asystole, and intraoperative death. The sympathetic nervous system and baroreceptor reflexes are not fully mature. The infant cardiovascular system displays a blunted response to exogenous catecholamines. The immature heart is more sensitive to depression by volatile anesthetics and to opioid-induced bradycardia. Infants are less able to respond to hypovolemia with compensatory vasoconstriction. Intravascular volume depletion in neonates and infants may be signaled by ...