Acute respiratory failure occurs when the pulmonary system is unable to maintain adequate gas exchange to meet metabolic demands. The resulting failure can be classified as hypercarbic (Paco2 >50 mm Hg in previously healthy children), hypoxemic (Pao2 <60 mm Hg in previously healthy children without an intracardiac shunt), or both. Hypoxemic respiratory failure is frequently caused by ventilation-perfusion mismatch (perfusion of lung that is not adequately ventilated) and shunting (deoxygenated blood bypasses ventilated alveoli). Hypercarbic respiratory failure results from inadequate alveolar ventilation secondary to decreased minute ventilation (tidal volume × respiratory rate) or an increase in dead space ventilation (ventilation of areas receiving no perfusion).
Respiratory failure may occur with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). The definitions of these are in the process of revision; however, currently ALI isdefined as having the following four clinical features: acute onset,bilateral pulmonary edema, no clinical evidence of elevated leftatrial pressure, and a ratio of Pao2 to Fio2 ≤ 300 mm Hg regardlessof the level of positive end-expiratory pressure (PEEP). ARDSis a subset of ALI with more severe hypoxemia (Pao2/Fio2 of ≤ 200 mm Hg). These syndromes can be triggered by a variety ofinsults, including sepsis, pneumonia, shock, burns, or traumaticinjury, all resulting in inflammation and increased vascular permeability leading to pulmonary edema. Numerous mediators ofinflammation (tumor necrosis factor, interferon-γ, nuclear factor κB, and adhesion molecules) may be involved in the development of ARDS. Surfactant action also may be affected.
Respiratory failure is frequently caused by bronchiolitis (often caused by respiratory syncytial virus), asthma, pneumonia, upper airway obstruction, and sepsis/ARDS. Respiratory failure requiring mechanical ventilation develops in 7% to 21% of patients hospitalized for respiratory syncytial virus.
Asthma is increasing in prevalence and is the most common reason for unplanned hospital admissions in children 3 to12 years of age in the United States. Environmental factors (exposure to cigarette smoke) and prior disease characteristics (severity of asthma, exercise intolerance, delayed start of therapy, andprevious intensive care unit admissions) affect hospitalizationand near-fatal episodes. The mortality rate of asthma for childrenyounger than 19 years of age has increased by nearly 80% since1980. Deaths are more common in African-American children.
Chronic respiratory failure (with acute exacerbations) is often due to chronic lung disease (bronchopulmonary dysplasia, cystic fibrosis), neurologic or neuromuscular abnormalities, and congenital anomalies.
Early signs of hypoxic respiratory failure include tachypnea and tachycardia in attempt to improve minute ventilation and cardiac output and to maintain delivery of oxygenated blood to the tissues. Further progression of disease may result in dyspnea, nasal flaring, grunting, use of accessory muscles of respiration, and diaphoresis. Late signs of inadequate oxygen delivery include cyanosis and altered mental status (initially confusion and agitation). Signs and symptoms of hypercarbic respiratory failure include attempts to increase minute ventilation (tachypnea and increased depth of breathing) and altered mental status (somnolence).