The respiratory system is comprised of lung parenchyma and compliant airways.
Flow limitation and elevated airway resistance induce flutter of the
airway wall that generates the high-pitched sounds known as wheezing.
Wheezing implies obstructive airway disease when diffuse, and focal obstruction
when localized. However, severe flow limitation may exist without
wheezing. Because intrathoracic airway lumen size normally increases
during inspiration and decreases during expiration, wheezing is generally
more prominent during expiration. Bronchiolitis is the most frequent
cause of wheezing in infants, and asthma is the most frequent cause
in children and adolescents.
Approximately 30% of children will have an illness associated
with wheezing by 3 years of age and 50% by 6 years of age.1 Most
children have benign, transient wheezing episodes that do not persist
beyond 6 years of age. These “early wheezers” may
have congenitally smaller airways that predispose them to wheezing
with viral illnesses during infancy and early childhood. Maternal
smoking is a risk factor for both transient and persistent wheezing.
However, the approximately 14% of children whose wheezing
appears before 3 years of age and persists at 6 years have additional
risk factors for asthma, including eczema, maternal asthma, and elevated
immunoglobulin E (IgE) levels during infancy.
This section includes a discussion of pulmonary anatomy, mechanics, and
physiology relevant to clinical assessment and management of the pediatric
patient with asthma, bronchiolitis, or other obstructive airway diseases
that cause wheezing.
The lungs consist of a supporting network of connective tissue
and a series of compliant tubes that become more numerous and more
narrow as they progressively branch peripherally. The cross-sectional
surface area of an airway is proportionate to the square of the
lumen radius. A decrease in airway radius exponentially diminishes
the lumen available for airflow. However, because the net cross-sectional
area of the tracheobronchial tree increases as these airways branch,
airway resistance progressively diminishes peripherally. The nasal
passages account for 50% of total airway resistance. Nasal
resistance may increase substantially in the presence of nasal mucus
or edema, a clinically important event, especially
in the infant with bronchiolitis. The conducting airways extend from
the trachea to the terminal bronchioles and do not participate in gas
exchange. More distally, the transitional and respiratory
zones have increasing numbers of alveoli and comprise the
Lung tissue has elastic properties, the tendency to resist deformation
or stretch with an opposing force that attempts to return the structure
to its former state. Any collapse or decompression of alveoli or
airways deforms adjacent tissue, which leads to elastic forces that
serve to reestablish and maintain airway patency. This relationship,
termed mechanical interdependence, promotes heterogeneous
lung emptying by maintaining airway patency until end expiration.
Forces of stretch and recoil are active on each lung as a unit
and on the chest wall. The resting state of these forces is generally
considered to be at functional residual capacity,
the lung volume at which the inherent outward elastic force of the
chest wall equals the inherent inward elastic recoil of the stretched
lung.2 An important consequence of elastic recoil is
the generation of force on the lung to contract when inflated above functional
residual capacity. The force required to stretch elastic tissue, and
the resulting opposite force generated by the elastic tissue itself,
is dependent on how far the tissue is stretched from this equilibrium
state. Normally, at functional residual capacity, the tissue is
relaxed at end expiration, and inspiration begins with minimal effort
at the onset of inspiratory muscle contraction. However, in the
presence of hyperinflation above functional residual capacity, this
inward elastic force (elastic recoil) must be overcome before a
breath can be initiated, a phenomenon referred to as auto–positive
end-expiratory pressure (auto-PEEP). So, in the presence
of hyperinflation, a greater negative inspiratory pressure needs
to be generated by the patient in order to initiate a breath.
lung is covered by visceral pleura, a serous membrane that adheres tightly
to the surface of the lung and forms a closed, invaginated sac.
It reflects upon itself to form the parietal pleura lining the inner
surface of the corresponding side of the mediastinum, chest wall,
and much of the diaphragm. The pleural space is a potential space
between the two layers of pleurae and contains a small amount of
fluid that allows the pleurae to slide across one another during
respiration. The structural arrangement of lung, mediastinal structures,
visceral and parietal pleurae, chest wall, and diaphragm comprises
a system in which any change in intrapleural pressure is transmitted
to the other structures.3 Important physiologic and
clinical consequences of this include the following:
1. The pleural space effectively couples the lung to the chest wall and
diaphragm and facilitates lung inflation as a result of negative
intrapleural pressure changes generated by chest wall and diaphragmatic
2. Positive intrapleural pressure, as occurs during forced exhalation,
exerts positive, compressive forces on airways that progressively
diminish airway lumen size as exhalation proceeds (dynamic airway
compression, see below).
3. Violation of the pleural space releases the outward forces imposed
by the chest wall, resulting in unopposed elastic recoil and lung
collapse (pneumothorax or hemothorax).
Inspiration is an active process aided by the diaphragm and external
intercostal muscles and, during exertion, by the accessory muscles
(scalene and sternocleidomastoid).2 Expiration
is normally a passive process, facilitated by elastic recoil of
the stretched lung. Positive pressure generated during relaxed expiration,
as a result of elastic recoil, compresses conducting airways and
decreases their lumen size in a homogeneous fashion down to functional
In the presence of diffuse (e.g., asthma, bronchiolitis) or focal
(e.g., foreign body) intrathoracic airway obstruction, the normally
passive process of expiration becomes active in an attempt to overcome
airway resistance. ...