540 Chapter 16
required for subsequent breaths. However, if the baby is pre-
mature and its lungs have not matured sufficiently to produce
surfactant, that effort must be duplicated with every breath.
Surfactant and Respiratory
Distress Syndrome
Alveolar fluid contains a substance that reduces surface tension.
This substance is called surfactant —a contraction of surface
active agent. Surfactant is secreted into the alveoli by type II
alveolar cells ( fig. 16.11 ), and consists of phospholipids—
primarily phosphatidylcholine and phosphatidylglycerol —together
with hydrophobic surfactant proteins. Surfactant becomes inter-
spersed between water molecules at the water– air interface; this
reduces the hydrogen bonds between water molecules (shown in
chapter 2, fig. 2.7) at the surface and thereby reduces the sur-
face tension. As a result of this effect of pulmonary surfactant,
the surface tension of the alveoli is negligible. The surfactant
secreted into the alveoli by type II alveolar cells is removed by
alveolar macrophages.
The ability of surfactant to lower surface tension improves
as the alveoli get smaller during expiration. This may be because
the surfactant molecules become more concentrated as the alve-
oli get smaller. Surfactant thus prevents the alveoli from col-
lapsing during expiration, as would be predicted from the law
of Laplace. Even after a forceful expiration, the alveoli remain
open and a residual volume of air remains in the lungs. Since the
alveoli do not collapse, less surface tension has to be overcome
to inflate them at the next inspiration.
Surfactant begins to be produced in late fetal life. Even so,
a normal newborn with partially collapsed alveoli must over-
come great surface tension forces to take the first breath of life;
it must create a transpulmonary pressure 15 to 20 times that
Figure 16.11 The production of pulmonary
surfactant. Produced by type II alveolar cells, surfactant
appears to be composed of a derivative of lecithin combined
with protein.
Surfactant
Alveolus
Macrophage
Type II
alveolar cell
Capillary
endothelium
Basal
lamina
Type I
alveolar cell
CLINICAL APPLICATION
Respiratory distress syndrome ( RDS ), where the alveoli
are collapsed in a neonate due to lack of surfactant, occurs
in 60% of babies born at less than 28 weeks of gestation
(normal pregnancy lasts 37 to 42 weeks), 30% of babies
born at 28 to 34 weeks, and less than 5% of babies born
after 34 weeks. Most of these babies can be saved by the
use of mechanical ventilators and by exogenous surfactant
delivered into the baby’s lungs by an endotracheal tube.
When the baby’s lungs are sufficiently mature, they manu-
facture their own surfactant.
People with lung injury caused by septic shock may
develop acute respiratory distress syndrome ( ARDS ).
Inflammation causes increased capillary and alveolar perme-
ability, producing a protein-rich fluid in the lungs. This reduces
lung compliance, and surfactant production, and the decreased
surfactant further reduces compliance. This produces hypox-
emia (low blood oxygen) of the blood leaving the lungs. Severe
hypoxemia can be fatal, but survival has improved in recent
years due to improvements in medical interventions.
LEARNING OUTCOMES
After studying this section, you should be able to:
- Explain how inspiration and expiration are
accomplished. - Describe lung volumes and capacities, and explain
how pulmonary function tests relate to pulmonary
disorders.
| CHECKPOINT
- Describe the changes in the intrapulmonary and
intrapleural pressures that occur during inspiration,
and use Boyle’s law to explain the reasons for these
changes.
4a. Explain how the compliance and elasticity of the
lungs affect inspiration and expiration.
4b. Describe pulmonary surfactant and discuss its
significance.
16.3 MECHANICS OF BREATHING
Normal, quiet inspiration results from muscle contraction,
and normal expiration from muscle relaxation and elastic
recoil. The amount of air inspired and expired can be mea-
sured in a number of ways to test pulmonary function.