Ganong's Review of Medical Physiology, 23rd Edition

598 SECTION VIIRespiratory Physiology

epithelial cells that secrete it. SP-B and SP-C are smaller pro-
teins, which facilitate formation of the monomolecular film of
phospholipid. A mutation of the gene for SP-C has been
reported to be associated with familial interstitial lung dis-
ease. Like SP-A, SP-D is a glycoprotein. Its full function is
uncertain. However, SP-A and SP-D are members of the col-
lectin family of proteins that are involved in innate immunity
in the conducting airway as well as in the alveoli. For other
roles of surfactant, see Clinical Box 35–2.

WORK OF BREATHING

Work is performed by the respiratory muscles in stretching the
elastic tissues of the chest wall and lungs (elastic work; approxi-
mately 65% of the total work), moving inelastic tissues (viscous
resistance; 7% of total), and moving air through the respiratory
passages (airway resistance; 28% of total). Because pressure
times volume (g/cm^2 × cm^3 = g × cm) has the same dimensions
as work (force × distance), the work of breathing can be calcu-
lated from the relaxation pressure curve (Figures 35–10 and
35–14). The total elastic work required for inspiration is repre-
sented by the area ABCA in Figure 35–14. Note that the relax-
ation pressure curve of the total respiratory system differs from
that of the lungs alone. The actual elastic work required to in-
crease the volume of the lungs alone is area ABDEA. The
amount of elastic work required to inflate the whole respiratory
system is less than the amount required to inflate the lungs
alone because part of the work comes from elastic energy stored
in the thorax. The elastic energy lost from the thorax (area
AFGBA) is equal to that gained by the lungs (area AEDCA).

FIGURE 35–13 Formation and metabolism of surfactant.
Lamellar bodies (LB) are formed in type II alveolar epithelial cells and
secreted by exocytosis into the fluid lining the alveoli. The released
lamellar body material is converted to tubular myelin (TM), and the TM
is the source of the phospholipid surface film (SF). Surfactant is taken
up by endocytosis into alveolar macrophages and type II epithelial
cells. N, nucleus; RER, rough endoplasmic reticulum; CB, composite
body. (Reproduced with permission from Wright JR: Metabolism and turnover of
lung surfactant. Am Rev Respir Dis 1987;136:426.)

RER

LB

CB

N

N

N

TM

Type II Golgi

cell

Type I cell

Alveolar

macrophage

Air space

SF

Fatty acids

Choline

Glycerol

Amino acids

Etc

CLINICAL BOX 35–2

Surfactant

Surfactant is important at birth. The fetus makes respiratory

movements in utero, but the lungs remain collapsed until

birth. After birth, the infant makes several strong inspira-

tory movements and the lungs expand. Surfactant keeps

them from collapsing again. Surfactant deficiency is an im-

portant cause of infant respiratory distress syndrome

(IRDS, also known as hyaline membrane disease), the seri-

ous pulmonary disease that develops in infants born before

their surfactant system is functional. Surface tension in the

lungs of these infants is high, and the alveoli are collapsed

in many areas (atelectasis). An additional factor in IRDS is

retention of fluid in the lungs. During fetal life, Cl– is se-

creted with fluid by the pulmonary epithelial cells. At birth,

there is a shift to Na+ absorption by these cells via the epi-

thelial Na+ channels (ENaCs), and fluid is absorbed with the

Na+. Prolonged immaturity of the ENaCs contributes to the

pulmonary abnormalities in IRDS.

Patchy atelectasis is also associated with surfactant defi-

ciency in patients who have undergone cardiac surgery in-

volving use of a pump oxygenator and interruption of the

pulmonary circulation. In addition, surfactant deficiency

may play a role in some of the abnormalities that develop

following occlusion of a main bronchus, occlusion of one

pulmonary artery, or long-term inhalation of 100% O 2. Cig-

arette smoking also decreases lung surfactant.

FIGURE 35–14 Relaxation pressure curves in the lung. The

relaxation pressure curves of the total respiratory system (PTR), the

lungs (PL), and the chest (PW) are plotted together with standard vol-

umes for functional residual capacity and tidal volume. The transmural

pressure is intrapulmonary pressure minus intrapleural pressure in the

case of the lungs, intrapleural pressure minus outside (barometric)

pressure in the case of the chest wall, and intrapulmonary pressure mi-

nus barometric pressure in the case of the total respiratory system.

From these curves, the total and actual elastic work associated with

breathing can be derived (see text). (Modified from Mines AH: Respiratory

Physiology, 3rd ed. Raven Press, 1993.)

6

4

2

0

− 20 0 + 20

BC

H

G

F

A E

D

Transmural pressure (cm H 2 O)

PW PL

PTR

Lung volume (L)