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To ventilate the lungs with fresh gas, the respiratory muscles must overcome the static-elastic and dynamic-resistive forces intrinsic to the lungs themselves. Changes in these opposing forces during postnatal development affect lung volume, the pattern of respiration, and the work of breathing.[96]
Lung compliance changes with age as a function of the changing alveolar structure, amount of elastin, and amount of surfactant.[97] At birth, compliance is low secondary to the presence of thick-walled alveolar precursors and decreased amounts of elastin. A deficiency of surfactant as seen in hyaline membrane disease further decreases compliance. Compliance improves over the first years of life with continuing development of alveoli and elastin.
The thoracic cage of the newborn is mechanically different from that of the adult. The chest wall in infants is less rigid because ribs are cartilaginous and not bony. In addition, the boxlike configuration of an infant's thorax permits less elastic recoil than the dorsoventrally flattened thoracic cage of the adult does.[98] There are also age-related differences in the intercostal and diaphragmatic muscle fibers. Adults have a high proportion of slow-twitch, high-oxidative, fatigue-resistant fibers: 65% of the intercostal fibers and 60% of the diaphragmatic fibers. Neonates have less: 19% to 46% of the intercostal fibers and 10% to 25% of the diaphragmatic fibers.[99] Therefore, an infant is more vulnerable to muscle fatigue, which may further decrease the stability of the chest wall. As a result of all these factors, an infant's chest wall is extremely compliant. The net effect of the compliant chest wall and the poorly compliant lungs should be alveolar collapse with lower resting lung volume or passive functional residual capacity (FRC). Despite this tendency to collapse, a child maintains a larger dynamic FRC by a number of active mechanisms, including incomplete exhalation secondary to a rapid respiratory rate, laryngeal breaking, and stabilization of the chest wall with increased intercostal tone during exhalation. [100] [101] [102] [103]
The upper airway of children and adults has numerous anatomic differences that must be considered before any airway manipulation is attempted. The more anterior and cephalad position of the larynx in children explains the advantage of the "sniffing position" for either mask ventilation or endotracheal intubation. Extreme neck extension can actually obstruct the airway. In addition, whereas the narrowest part of the adult airway is at the level of the vocal cords, a child's airway is narrowest at the level of the cricoid cartilage. An endotracheal tube (ETT) that passes easily through the vocal cords may cause ischemic damage to the airway more distally. The cricoid narrowing and the very pliant tracheal cartilage provide an adequate seal around an uncuffed ETT. Children younger than 8 years rarely require a cuffed ETT.[104]
The elastic properties of the lung are also closely correlated with closing capacity. Closing volume is the lung volume at which the terminal airways begin to collapse and a discontinuity is created between trapped gas and conducting airways.[105] Large closing volumes increase dead-space ventilation and can lead to atelectasis and shunting. It is postulated that the elastic tissue helps keep the airways open, so the greater the elastic stroma in the small airways, the lower the lung volume required before gravitational forces can close small, noncartilaginous airways. Therefore, closing volume is small in late adolescents and relatively large in the elderly and the very young.[106] Children overcome the complications of large closing volumes and secondary atelectasis by keeping their lungs expanded through constant activity and crying. However, closing volume becomes a significant problem in an infant who is inactive or sedated because of illness.
Poiseuille's law defines resistance during laminar flow through
a tube:
Resistance = 81η/π4
where l is the length of the tube, r is the radius, and η is gas viscosity.
Because airflow in the lung is generally not laminar, resistance is underestimated
by this calculation. However, the Poiseuille law does emphasize dependence on the
radius of the airway.[107]
Not surprisingly, neonates have small airways with high resistance or low conductance (conductance = 1/resistance). Of interest, the caliber of the small airways does not significantly increase until after the age of 5 years; hence, young children have elevated resistance at baseline and are particularly vulnerable to diseases that cause further narrowing of the airways (i.e., smooth muscle constriction, airway edema/inflammation).[108]
Respiratory control in a newborn infant may be unique. Hypoxia in a newborn produces an initial increase, followed by a sustained decrease in ventilation. [109] This response is more exaggerated in preterm newborns and disappears rapidly in full-term infants after several weeks. Irregular respiration, known as periodic breathing, is also more common in infants, particularly in the preterm, a finding suggesting incomplete development of the medullary respiratory centers.[110]
Fetal hemoglobin does not bind with 2,3-diphosphoglycerate (2,3-DPG), so the oxygen half-saturation pressure (P50 ) of fetal hemoglobin is lower than that of adult hemoglobin in the presence of 2,3-DPG.[111] This lower P50 gives the fetus the teleologic advantage of loading more oxygen at low fetal oxygen tensions (fetal PaO2 , 20 to 30 mm Hg). As fetal hemoglobin is replaced by adult hemoglobin, a young infant's P50 approximates an adult's, thereby enhancing oxygen delivery. At 3 to 4 months of age, infants have higher levels of 2,3-DPG than adults do.[112] The resultant higher P50 may compensate for the relative anemia at this age, when the hemoglobin concentration commonly falls below 10 g/dL.
An infant is a very metabolically active organism: oxygen consumption at birth is 6 to 8 mL/kg/min and falls to 5 to 6 mL/kg/min over the first year of life.[113] The decreased ventilation-perfusion ratio, the decreased P50 of fetal hemoglobin, and the physiologic anemia characteristic of infants can make adequate oxygen delivery difficult. The infant compensates by having high cardiac output up to 250 mL/kg/min, which remains elevated until 4 to 5 months of age.[114] When oxygen delivery to tissues is inadequate, the cells shift to anaerobic metabolism through the Embden-Meyerhof glycolytic pathway. By-products of this pathway are lactic and pyruvic acid, which produce a net acid load. Thus, arterial pH (pHa ) becomes a very sensitive indicator of the adequacy of oxygen transport. Particularly in young infants and children, metabolic acidosis indicates inadequate oxygen transport until proved otherwise.
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