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Respiratory distress results from dysfunction or disruption of the respiratory tract and/or systems that control or modulate respiration Respiratory failure is the inability to meet the metabolic demand for O2 (hypoxia) or to eliminate CO2 (hypercapnia) Criteria for defining respiratory failure vary widely; one set of criteria is presented in Table 71.1 Hypoxia can be categorized on the basis of mechanism Arterial hypoxemia results from an inability to deliver adequate O2 to the blood, low atmospheric PO2 , diffusion impairment, anatomic or physiologic shunt, or increased metabolic demand Anemic hypoxia is the result of the blood’s inability to deliver adequate O2 to tissues as a result of decreased hemoglobin oxygen-carrying capacity Hypokinetic, ischemic, or stagnant hypoxia also results in an inability of the blood to transport O2 to the tissues Histotoxic hypoxia results from inability to metabolize O2 at the tissue level as a result Hypercapnia often contributes to respiratory failure as a result of hypoxemia and is less commonly the primary cause Infants are at an increased risk of respiratory distress compared with children and adults because of anatomic and physiologic differences ( Table 71.2 ) These differences result in greater risk of airway obstruction, less efficient respiratory effort, limited respiratory reserve, and dysfunction of CNS respiratory control DIFFERENTIAL DIAGNOSIS Establishing a diagnosis for respiratory distress in part depends on localizing the pathology to a particular organ system In addition to primary respiratory etiologies, disease or dysfunction of other organ systems may indirectly result in respiratory disturbance by compromising respiratory system function or by stimulating compensatory respiratory mechanisms ( Tables 71.3 to 71.5 ) Treatment of the underlying cause is essential for definitive treatment of the respiratory distress Respiratory System Respiratory distress may be caused by upper or lower airway obstruction or by disorders of the parenchyma or interstitium Upper airway obstruction is common in infants and young children in part because of their airway anatomy and physiology (see Chapter 75 Stridor ) The hallmark of complete upper airway obstruction is inability to phonate (i.e., no speech, cry, or cough) Manifestations of upper airway obstruction may also include nasal flaring, stertor or snoring, gurgling, drooling, dysphagia, hoarseness, stridor, retractions, and paradoxical chest/abdominal wall movement In neonates, common causes include nasal
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