RESPIRATORY SYSTEM
Age-Dependent Respiratory Variables: Structural and
Functional Development
Airways and Alveoli
The main fetal organs, including the lungs, appear in the fourth
to eighth weeks of gestation ( Table
76-7
; see Chapter 59
and Chapter 60
).[5]
At 4 weeks, the endodermal lung buds have divided into the main stem bronchi; by
6 weeks, all subsegmental bronchi can be identified, and by 16 weeks, the number
of airway generations arising from axial pathways is similar to that in adults.
When this airway development is complete, the terminal airways remodel and multiply
to form a cluster of large saccules, which are alveolar precursors capable of supporting
gas exchange. True alveoli appear before and after birth, when the respiratory saccules
become thinner and septated during postnatal growth.[82]
At birth, children have 24 million alveoli; by 8 years, this number
has increased to 300 million. After this age, further lung growth reflects an increase
in size of the alveoli. Collateral ventilation between airways (Lambert's canals)
and between alveoli (Kohn's pores) is not present at birth but develops by age 8.
[83]
The neonatal lung has a decreased amount of elastic tissue, with
elastin extending only to the level of the alveolar duct. Elastin progresses to
the level of the alveolus and reaches maximal levels by 18 years of age; over the
next 5 decades, it slowly deteriorates.[84]
Lung
compliance is integrally related to the amount of elastin, and hence compliance peaks
in adolescence and is relatively low in the very young and the very old.
TABLE 76-7 -- Age-dependent respiratory variables: normal values
*
|
Newborn |
6 mo |
12 mo |
3 yr |
5 yr |
12 yr |
Adult |
|
Respiratory rate (breaths/min) |
50 ± 10 |
30 ± 5 |
24 ± 6 |
24 ± 6 |
23 ± 5 |
18 ± 5 |
12 ± 3 |
|
Tidal volume (mL) |
21 |
45 |
78 |
112 |
270 |
480 |
575 |
|
Minute ventilation (L/min) |
1.05 |
1.35 |
1.78 |
2.46 |
5.5 |
6.2 |
6.4 |
|
Alveolar ventilation (mL/min) |
385 |
— |
1245 |
1760 |
1800 |
3000 |
3100 |
|
Dead space-tidal volume ratio |
0.3 |
0.3 |
0.3 |
0.3 |
0.3 |
0.3 |
0.3 |
|
Oxygen consumption (mL/kg/min) |
6 ± 0.9 |
5 ± 0.9 |
5.2 ± 0.9 |
— |
6.0 ± 1.1 |
3.3 ± 0.6 |
3.4 ± 0.6 |
|
Vital capacity (mL) |
120 |
— |
— |
870 |
1160 |
3100 |
4000 |
|
Functional residual capacity (mL) |
80 |
— |
— |
490 |
680 |
1970 |
3000 |
|
Total lung capacity (mL) |
160 |
— |
— |
1100 |
1500 |
4000 |
6000 |
|
Closing volume as percentage of vital capacity |
— |
— |
— |
— |
20 |
8 |
4 |
|
Number of alveoli (saccules) × 106
|
30 |
112 |
129 |
257 |
280 |
— |
300 |
|
Specific compliance: CL/FRC (mL/cm H2
O/L) |
0.04 |
0.038 |
— |
— |
0.06 |
— |
0.05 |
|
Specific conductance of small airways (mL/sec/cm H2
O/g) |
0.02 |
— |
3.1 |
1.7 |
0.12 |
8.2 |
13.4 |
|
Hematocrit |
55 ± 7 |
37 ± 3 |
35 ± 2.5 |
40 ± 3 |
40 ± 2 |
42 ± 2 |
43–48 |
|
pHa
|
7.30 ± 7.40 |
— |
7.35–7.45 |
— |
— |
— |
7.35–7.45 |
|
PaCO2
(mm Hg) |
30–35 |
— |
30–40 |
— |
— |
— |
30–40 |
|
PaO2
(mm Hg) |
60–90 |
— |
80–100 |
— |
— |
— |
80–100 |
|
From O'Rourke PP, Crone RK: The respiratory system.
In Gregory G (ed): Pediatric Anesthesia, 2nd ed.
New York, Churchill Livingstone, 1989, p 63. |
*Also
see Chapter 60
.
Pulmonary Circulation
The main axial arteries are present at 14 weeks' gestation, and
by 20 weeks, the pattern of branching is similar to that seen in adults. By 20 weeks'
gestation, collateral supernumerary vessels are present in an adult pattern. During
fetal life, additional arteries develop to accompany the respiratory airways and
saccules. Bronchial arteries appear between the 9th and 12th weeks of gestation.
[85]
The arterial wall develops a fine elastic
lamina
by 12 weeks' gestation, and muscle cells develop as early as 14 weeks.[86]
By 19 weeks, the elastic structure extends to the seventh generation of arterial
branching, and muscularization extends distally. In the fetus, muscularization of
the arteries ends at a more proximal level than in childhood or adulthood. However,
the arteries that are muscularized have thicker walls than the arteries of similar
size in an adult. The pattern of development of the pulmonary venous system is similar
to that of the arterial system.[82]
Studies of
blood flow to the lungs of fetal lambs suggest that the pulmonary arteries are in
a state of active vasoconstriction until the latter part of gestation. In the fetal
lamb, pulmonary blood flow at 0.4 to 0.7 gestation is only 3.5% of the combined ventricular
output, but it increases to 7% near term.[87]
The pulmonary arteries continue to develop after birth; new artery
formation follows airway branching up to 19 months of age, and supernumerary arteries
continue to grow until the eighth year.[88]
As
alveolar size increases, the acinar branching pattern becomes more extensive and
complex.[82]
The arterial structure also changes:
preexisting arteries increase in size, and during the first year of life, the thickness
of the muscular arteries decreases to adult levels.
Biochemical Development
In the developing lung, two cellular types become obvious by 24
weeks' gestation as alveolar cuboidal epithelium flattens: type I pneumocytes, which
become lining and supporting cells for alveoli, and the larger type II cells, which
manufacture and store surfactant.[89]
Surfactant
initially appears at 23 to 24 weeks' gestation in humans and increases in concentration
during the last 10 weeks of gestational life.[90]
Maturation of the surfactant system is partly controlled by the neuroendocrine system.
[91]
Respiratory Transition: Placenta to Lung
By approximately 24 weeks' gestation, the lungs are capable of
extrauterine gas exchange. However, several important circulatory and mechanical
changes must occur soon after birth for pulmonary gas exchange to be adequate.
Ventilation begins to match perfusion within the first hours of
life. Initially, there is right-to-left intrapulmonary shunting through atelectatic
areas in the lung, as well as possible extrapulmonary shunting through the ductus
arteriosus and foramen ovale. The resultant PaO2
of 50 to 70 mm Hg in the newborn infant indicates a right-to-left shunt three times
that seen in normal adults.[92]
[93]
The transition from fetal to neonatal respiration and circulation
is dynamic. Postnatally, the pulmonary vascular bed can continue to constrict in
response to physiologic stresses such as acidosis or hypoxia. If constriction
does occur, the extrapulmonary right-to-left shunting of desaturated blood through
the foramen ovale and the ductus arteriosus increases, thus decreasing pulmonary
blood flow.[94]
Persistence of this active pulmonary
vasoconstriction is called persistent pulmonary hypertension of the newborn or persistent
fetal circulation. This syndrome is an important consideration when treating infants
with congenital diaphragmatic hernia, meconium aspiration, and sepsis.[95]
