Gas exchange depends on alveolar ventilation, pulmonary capillary blood flow, and the diffusion of gases across the alveolar-capillary membrane. Exchange of CO2 is determined by alveolar ventilation, whereas the exchange of O2 is influenced primarily by the regional matching of ventilation (V) with pulmonary blood flow (Q) (V/Q matching). V/Q matching is maintained, in part, by hypoxic pulmonary vasoconstriction (local constriction of the pulmonary vessels in areas that are hypoventilated). There are five causes of hypoxemia (Table 133-1). Disorders resulting in V/Q mismatching (such as pneumonia and atelectasis) are the most common causes of hypoxemia.
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The lungs are constantly exposed to particles and infectious agents. The nose is the primary filter for large particles. The ciliated epithelium of the paranasal sinuses and nasal turbinates move filtered particles toward the pharynx. Particles less than 10 μm in diameter may reach the trachea and bronchi and deposit on the mucosa. Particles less than 1 μm may reach the alveoli. Ciliated cells lining the airways from the larynx to the bronchioles continuously propel a thin layer of mucus toward the mouth. Alveolar macrophages and polymorphonuclear cells engulf particles and pathogens that have been opsonized by locally secreted IgA antibodies or transudated serum antibodies.
Cough, important in protecting the lungs, is a forcefulexpiration that can clear the airways of debris and secretions.Cough may be voluntary or generated by reflex irritation ofthe nose, sinus, pharynx, larynx, trachea, bronchi, or bronchioles. Effective cough requires the ability to (1) inhale to near total lung capacity, (2) close and open the glottis, and (3) contract abdominal muscles to forcibly exhale. Loss of theability to cough, as with neuromuscular weakness, results in poor secretion clearance and predisposes to atelectasis andpneumonia.
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The complete respiratory history includes onset, duration, and frequency of respiratory symptoms (cough, noisy breathing, work of breathing/exercise tolerance, nasal congestion, sputum production), swallowing function (especially in infants), and exposure to others with respiratory illness. It is important to obtain information concerning the severity (hospitalizations, emergency department visits, missed school days) and pattern (acute, chronic, or intermittent) of symptoms. For infants, a feeding history should be obtained, including questions of coughing or choking with feeds. Family history should include questions about asthma and atopy, immune deficiencies, and CF. The environmental historyqueries exposure to smoke, pets, and pollutants. Travel history may also be relevant.
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Clothing should be removed from the upper half of the child’s body so that the thorax may be inspected, although maintaining modesty for adolescents should be respected. It is optimal to observe the respiratory pattern, rate, and work of breathing while the child is quiet, noting the shape and symmetry of the chest wall and the anteroposterior (AP) diameter.
Any factor that impairs respiratory mechanics is likely to increase the respiratory rate. However, nonrespiratory causes of tachypnea include fever, pain, and anxiety. Respiratory rates vary with age and activity (Table 133-2).
It is important to observe the respiratory pattern and degree of effort (work of breathing). Hyperpnea (increased depth of respiration) may be observed with fever, metabolic acidosis, pulmonary and cardiac disease, or extreme anxiety. Hyperpnea without signs of respiratory distress suggests an extrapulmonary etiology (metabolic acidosis, fever, pain). Increased work of breathing can be described as inspiratory (intercostal, supraclavicular, or substernal retractions) or