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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.
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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.
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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.
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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
gas-exchanging units.
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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.
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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 ...