C h a p t e r 2 1
Control of Respiratory Function
523
the collagen fibers resist stretching and make lung infla-
tion more difficult. In lung diseases such as interstitial
lung disease and pulmonary fibrosis, the lungs become
stiff and noncompliant as the elastin fibers are replaced
with the collagen fibers of scar tissue. Pulmonary con-
gestion and edema produce a reversible decrease in pul-
monary compliance by increasing the water content of
the lung.
Elastic recoil
describes the ability of the elastic com-
ponents of the stretched or inflated lung to return to
their original position after having been stretched.
Overstretching lung tissues, as occurs with emphysema,
causes the elastic components of the lung to lose their
recoil, making the lung more compliant and easier to
inflate but more difficult to deflate because of its inabil-
ity to recoil.
Surface Tension.
An important factor in lung compli-
ance is the
surface tension
in the alveoli. The alveoli are
lined with a thin film of liquid, and it is at the interface
between this liquid film and the alveolar air that surface
tension develops. This can be explained by the fact that
the forces that hold the liquid molecules together are
stronger than those that hold the air molecules together.
In the alveoli, excess surface tension causes the liquid
film to contract, making lung inflation more difficult.
The relationship between the pressure within a sphere
such as an alveolus and the tension in the wall can be
described using the law of Laplace (pressure = 2 × sur-
face tension/radius). If the surface tension were equal
throughout the lungs, the alveoli with the smallest radii
would have the greatest pressure, and this would cause
them to empty into the larger alveoli (Fig. 21-12A). The
reason this does not occur is because of the surface ten-
sion-lowering molecules, called
surfactant
, that line the
inner surface of the alveoli.
Pulmonary surfactants, particularly surfactant B, exert
several important effects on lung inflation. They decrease
alveolar surface tension, thereby increasing lung compli-
ance and ease of inflation. Without this, lung inflation
would be extremely difficult. In addition, surfactant helps
to keep the alveoli dry and prevents the development of
pulmonary edema. This is because water is pulled out of
the pulmonary capillaries into the alveoli when increased
surface tension causes the alveoli to recoil.
Surfactants also stabilize alveolar inflation by chang-
ing their density in relation to alveolar size, with the sur-
factant molecules becoming more tightly compressed in
the small alveoli with their higher surface tension and
less compressed in the larger alveoli with their lower
surface tension (Fig. 21-12B). At low lung volumes, the
molecules become tightly packed, and at higher lung vol-
umes they spread out to cover the alveolar surface. In
surgical patients and bed-ridden persons, shallow and
quiet breathing often impairs the spreading of surfactant.
Encouraging these persons to cough and deep breathe
enhances the spreading of surfactant, allowing for a more
even distribution of ventilation and prevention of atelec-
tasis (incomplete expansion of a portion of the lung).
The type II alveolar cells that produce surfactant
do not begin to mature until the 26th to 27th week
Airways
Alveolus
Alveolus
P = 2 T/r
Radius = 1
Surface tension = T
Radius = 2
Surface tension = T
Surfactant film
(thicker in small alveolus;
thinner in larger alveolus)
A
B
C
Surfactant molecule
Palmitate
Glycerol
Phosphate
Choline
Hydrophobic
(nonpolar) part
Hydrophilic
(polar) part
Air
Liquid
Air
Liquid
FIGURE 21-12.
(A)
The effect of the surface tension (forces
generated at the fluid-air interface) and radius on the
pressure and movement of gases in the alveolar structures.
According to the law of Laplace (P = 2T/r, P = pressure,
T = tension, r = radius), the pressure generated within the
sphere is inversely proportional to the radius. Air moves from
the alveolus with a small radius and higher pressure to the
alveolus with the larger radius and lower pressure.
(B)
The
surfactant molecules with their hydrophilic heads (that attach
to the fluid lining of the alveolus) and their hydrophobic tails
(that are oriented toward the air interface.
(C)
The surfactant
molecules form a monolayer (shaded in blue) that disrupts
the intermolecular forces and lowers the surface tension
more in the smaller alveolus with its higher concentration
of surfactant than in the larger alveolus with its lower
concentration of surfactant.
