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Wheezing is a high-pitched sound that occurs when there is an elevation of airway resistance due to an obstructive process. The clinician must differentiate between stridor and wheeze because this determines location of the airway obstruction. Stridor is a sign of upper airway obstruction (above the thoracic inlet) that is more marked during inspiration, whereas wheeze signifies lower airway obstruction distal to the thoracic inlet that is more marked during expiration (see chapter 123, "Stridor and Drooling in Infants and Children").1-4 Wheezing implies a generalized obstructive airway disease when diffuse and focal obstruction when localized. However, severe flow limitation may exist without wheezing, for example, the silent chest in a severe asthma exacerbation. Bronchiolitis is the most frequent cause of wheezing in infants, and asthma is the most frequent cause in children and adolescents.


The nasal passages account for 50% of total airway resistance. Nasal resistance increases in the presence of nasal mucus or edema and may be clinically important in the infant with bronchiolitis. The conducting airways extend from the trachea to the terminal bronchioles and do not participate in gas exchange. The distal transitional and respiratory zones are the gas-exchanging units.

Lung tissue has elastic properties; functional residual capacity is the resting balance of stretch and recoil forces. 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. Inspiration is an active process generated by the diaphragm and external intercostal muscles. During exertion, inspiration is aided by the use of accessory muscles including scalene and sternocleidomastoid muscles.5 Expiration is normally a passive process, facilitated by elastic recoil of the stretched lung.

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. Abdominal and internal intercostal muscles are recruited. Positive intrapleural pressure is generated, and increasing external pressure is applied to the airways. This leads to progressively increasing airway obstruction as expiration proceeds, a phenomenon referred to as dynamic airway compression (Figure 124–1).6

FIGURE 124–1.

Normal inspiration and expiration (A, B) and dynamic airway compression (C) with development of auto–positive end-expiratory pressure (Auto-PEEP).

Dynamic airway compression results in prolonged expiratory time. The net result is failure of alveoli and distal airways to fully empty at end expiration, resulting in air trapping and increased functional residual capacity. Before subsequent inspiratory flow can begin, inspiratory muscles must overcome this increased elastic recoil, which substantially increases the work of breathing, a phenomenon referred to as auto–positive end-expiratory pressure. Finally, air trapping and subsequent atelectasis result in areas with ventilation–perfusion mismatch and hypoxemia.


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