Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 35

Pulmonary Function 595

COMPLIANCE OF THE

LUNGS & CHEST WALL

The interaction between the recoil of the lungs and recoil of
the chest can be demonstrated in living subjects through a
spirometer that has a valve just beyond the mouthpiece. The
mouthpiece contains a pressure-measuring device. After the
subject inhales a given amount, the valve is shut, closing off
the airway. The respiratory muscles are then relaxed while the
pressure in the airway is recorded. The procedure is repeated
after inhaling or actively exhaling various volumes. The curve
of airway pressure obtained in this way, plotted against vol-
ume, is the
relaxation pressure curve
of the total respiratory
system (Figure 35–10). The pressure is zero at a lung volume
that corresponds to the volume of gas in the lungs at the end
of quiet expiration (
functional residual capacity,
or
FRC;

also known as relaxation volume). It is positive at greater vol-

umes and negative at smaller volumes. The change in lung vol-

ume per unit change in airway pressure (

Δ

V/

Δ

P) is the

compliance

(stretchability) of the lungs and chest wall. It is

normally measured in the pressure range where the relaxation

pressure curve is steepest, and the normal value is approxi-

mately 0.2 L/cm H

2

O. However, compliance depends on lung

volume; an individual with only one lung has approximately

half the

Δ

V for a given

Δ

P. Compliance is also slightly greater

when measured during deflation than when measured during

inflation. Consequently, it is more informative to examine the

whole pressure–volume curve. The curve is shifted downward

and to the right (compliance is decreased) by pulmonary con-

gestion and interstitial pulmonary fibrosis (Figure 35–11).

Pulmonary fibrosis is a progressive restrictive airway disease

of unknown cause in which there is stiffening and scarring of

CLINICAL BOX 35–1

Airway Diseases That Alter Airflow

Obstructive Disease: Asthma

in the number of pulmonary alveolar macrophages, and these

macrophages release a chemical substance that attracts leu-

kocytes to the lungs. The leukocytes in turn release proteases

including elastase, which attacks the elastic tissue in the

lungs. At the same time,

α

1

-antitrypsin, a plasma protein that

normally inactivates elastase and other proteases, is itself in-

hibited. The

α

1

-antitrypsin is inactivated by oxygen radicals,

and these are released by the leukocytes. The final result is a

protease–antiprotease imbalance with increased destruction

of lung tissue. Similar protease–antiprotease imbalance can

occur through congenital deficiency α 1 -antitrypsin.

Airflow Measurements of Obstructive

& Restrictive Disease

In a healthy normal adult male, FVC is approximately 5.0 L, FEV 1

is approximately 4.0 L, and thus, the calculated FEV 1 /FVC is

80%. As would be expected, patients with obstructive or re-

strictive diseases display reduced FVC, on the order of 3.0 L, and

this measurement alone does not differentiate between the

two. However, measurement of FEV 1 can significantly vary be-

tween the two diseases. In obstructive disorders, patients tend

to show a slow, steady slope to the FVC, resulting in a small

FEV 1 , on the order of 1.3 L. However, in the restrictive disorder

patients, air flow tends to be fast at first, and then due to the

loss of elasticity, quickly levels out to approach FVC. The resul-

tant FEV 1 is much greater, on the order of 2.8 L, even though

FVC is equivalent. A quick calculation of FEV 1 /FVC for obstruc-

tive (42%) versus restrictive (90%) patients defines the hallmark

measurements in evaluating these two diseases. Obstructive

disorders result in a marked decrease in both FVC and FEV 1 /

FVC, whereas restrictive disorders result in a loss of FVC without

loss in FEV 1 /FVC.

Asthma is characterized by episodic or chronic wheezing,

cough, and a feeling of tightness in the chest as a result of

bronchoconstriction. Although the disease is not fully under-

stood, three airway abnormalities are present: airway ob-

struction that is at least partially reversible, airway inflamma-

tion, and airway hyperresponsiveness to a variety of stimuli. A

link to allergy has long been recognized, and plasma IgE le-

vels are often elevated. Proteins released from eosinophils in

the inflammatory reaction may damage the airway epithe-

lium and contribute to the hyperresponsiveness. Leuko-

trienes are released from eosinophils and mast cells, and can

enhance bronchoconstriction. Numerous other amines, neu-

ropeptides, chemokines, and interleukins have effects on

bronchial smooth muscle or produce inflammation, and they

may be involved in asthma.

Because β 2 -adrenergic receptors mediate bronchodilation,

β 2 -adrenergic agonists have long been the mainstay of treat-

ment for mild to moderate asthma attacks. Inhaled and sys-

temic steroids are used even in mild to moderate cases to re-

duce inflammation; they are very effective, but their side

effects can be a problem. Agents that block synthesis of leu-

kotrienes or their CysLT 1 receptor have also proved useful in

some cases.

Restrictive Disease: Emphysema

Emphysema is a degenerative and potentially fatal pulmo-

nary disease that is characterized by a loss of lung elasticity

and replacement of alveoli with large air sacs. This loss of elas-

ticity prevents full expansion of the lung, or airway restric-

tion, during breathing. The most common cause of emphy-

sema is heavy cigarette smoking. The smoke causes an increase