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CHAPTER 3

Respiratory Physiology and Support

John R. Gosche
Mark W. Newton
Laura Boomer

Introduction continues well after birth, however, so infants with adequate initial
The primary function of the lung is to exchange gases between the lung parenchyma to support extrauterine life may ultimately be left
bloodstream and the environment. The anatomy and physiologic con- with little or no functional impairment.
trol mechanisms of the lung and its associated pulmonary circulation Surfactant production in the foetal lung begins at about 20 weeks
allow for optimal efficiency of gas exchange. Due to a need for brevity, of gestation, but is not secreted by the lung until about 30 weeks
this chapter addresses only the features of lung development and pul- gestation. Surfactant consists of about 90% glycerophospholipids,
monary physiology that may impact the care of infants and children. of which dipalmitoylphosphatidyl choline (DPPC) is the most
The publications listed in the Suggested Reading at the end of this chap- important. During late gestation, the ratio of phosphatidyl choline
ter present a more in-depth understanding of pulmonary physiology, (PC, or lecithin) to other lipid components (phosphatidylglycerol,
sphingomyelin) changes, and thus the ratio of the different lipid
Pulmonary Physiology in the Neonate components of surfactant in the amniotic fluid can be used as an
Several unique aspects of neonatal pulmonary physiology related to index of lung maturity; that is, a lecithin/sphingomyelin (L/S) ratio
lung maturation and growth as well as the transition from intrauterine >2.0, which normally occurs around 35 weeks gestation and is
to extrauterine life may significantly complicate management of the associated with a low risk of respiratory distress syndrome (RDS).
surgical neonate. Infants born prior to the age of lung maturity are prone to atelectasis
The structure of the bronchial tree is established by the 16th week and pulmonary oedema due to a relative lack of surfactant, which can
of gestation, but alveolar maturation and growth continues throughout result in the development of hyaline membrane disease.
foetal life and into adulthood. Prenatal lung development is divided Foetal lung maturation and surfactant production can also be
into four phases: affected by hormonal influences. Foetal stress associated with
1. embryonic phase (3rd through 6th weeks of gestation), during uteroplacental insufficiency accelerates lung maturation, probably as
which the primitive lung bud forms; a result of the influence of elevated glucocorticoids and catecholamine
2. pseudoglandular phase (7th through 16th weeks of gestation), levels, resulting in a relatively low incidence of RDS in these infants.
during which the bronchial airways are established; Elevated insulin levels, however, inhibit surfactant production.
Thus, even term infants of diabetic mothers may be prone to the
3. canalicular phase (16th through 24th weeks of gestation), during
development of RDS.
which the structure of the distal airways and early vascularisation is
Due to the relatively greater tissue thickness in the normal newborn
established; and
lung, lung compliance in the neonate is approximately equal to that of
4. terminal saccular phase (24th week of gestation to term), during the adult. The chest wall of the newborn, however, is more compliant.
which primitive alveoli are formed and surfactant production begins. Thus, the intrapleural pressure in the newborn is less negative (i.e.,
only slightly less than atmospheric pressure) than in adults. Given
Throughout the period of prenatal lung development, interstitial
this relationship, one would expect the functional residual capacity
tissue gradually decreases, resulting in thinning of the walls of the
(FRC) to be lower in the neonate than in the adult. However, the
future alveoli. Even at birth, however, the lung does not contain
newborn infant augments FRC by maintaining inspiratory muscle
mature alveoli; instead, it has approximately 20 million primitive
activity throughout expiration thereby splinting the chest wall, and by
terminal sacs. Postnatally, the relatively shallow, cup-like terminal
increasing airway resistance via glottic narrowing during expiration.
saccules of the newborn lung gradually assume the more spherical,
As a result, the percent FRC of the neonate is similar to that of adults.
thin-walled structure of mature alveoli. In addition, new alveoli
Lung expansion and intrapleural pressures affect airway diameters
continue to develop up to 8 years of age. at which time approximately
and thus airway resistance. With forceful expiration, increased
300 million alveoli are present. After 8 years of age, lung growth is
intrapleural pressure compresses the airways, thus restricting air
associated with increases in alveolar size but not number.
flow and potentially causing air trapping. In the lung of the adult and
Lung hypoplasia is frequently associated with congenital surgical
older child, cartilaginous support of the airways prevents complete
anomalies such as congenital diaphragmatic hernia or congenital
airway collapse. Less cartilaginous support of the central airways in
cystic adenomatoid malformation that limit lung growth due to
premature infants, however, may result in air trapping during periods
compression of the developing lung. Furthermore, because late foetal
of increased respiratory effort.
lung growth is stimulated by rhythmic lung expansion associated
Haemoglobin in the foetus has a higher oxygen affinity than the
with foetal breathing, lung hypoplasia may also be associated with
haemoglobin found in the normal older child and adult. The increased
conditions that limit amniotic fluid volume (e.g., renal agenesis) and
oxygen affinity of foetal haemoglobin appears to be primarily due to a
in patients with severe neurologic abnormalities (e.g., anencephaly).
decreased affinity for 2,3-DPG. This increased oxygen affinity allows
New bronchial development does not occur after the 18th week
for greater uptake of oxygen from the placenta at the lower oxygen
of gestation, so infants who experienced early inhibition of lung
tensions normally observed in the foetus. Greater oxygen uptake
development will not develop completely normal lungs. Lung growth
also reflects higher foetal haemoglobin concentrations. Postnatally,