A chest radiograph may show evidence of the etiology ofrespiratory failure. The detection of atelectasis, hyperinflation, infiltrates, or pneumothoraces assists with ongoingmanagement. Diffuse infiltrates or pulmonary edema maysuggest ARDS. The chest radiograph may be normal whenupper airway obstruction or impaired respiratory controlsare the etiology. In patients presenting with stridor or otherevidence of upper airway obstruction, a lateral neck filmor computed tomography (CT) may delineate anatomicdefects. Direct visualization through flexible bronchoscopy allows identification of dynamic abnormalities of theanatomic airway. Helical CT helps diagnose a pulmonaryembolus.
Pulse oximetry allows noninvasive, continuous assessment of oxygenation but is unable to provide information about ventilation abnormalities. Determination of CO2 levels requires a blood gas measurement (arterial, venous, or capillary). An arterial blood gas allows measurement of CO2 levels and analysis of the severity of oxygenation defect through calculation of an alveolar-arterial oxygen difference. A normal Pco2 in a patient who is hyperventilating should heighten concern about the risk of further deterioration.
Hypoxic respiratory failure resulting from impairment of alveolar-capillary function is seen in ARDS; cardiogenic pulmonary edema; interstitial lung disease; aspiration pneumonia; bronchiolitis; bacterial, fungal, or viral pneumonia; and sepsis. It also can be due to intracardiac or intrapulmonary shunting seen with atelectasis and embolism.
Hypercarbic respiratory failure can occur when the respiratory center fails as a result of drug use (opioids, barbiturates, anesthetic agents), neurologic or neuromuscular junction abnormalities (cervical spine trauma, demyelinating diseases, anterior horn cell disease, botulism), chest wallinjuries, or diseases that cause increased resistance to airflow(croup, vocal cord paralysis, post-extubation edema). Maintenance of ventilation requires adequate function of the chestwall and diaphragm. Disorders of the neuromuscular pathways, such as muscular dystrophy, myasthenia gravis, andbotulism, result in inadequate chest wall movement, development of atelectasis, and respiratory failure. Scoliosis rarelyresults in significant chest deformity that leads to restrictivepulmonary function. Similar impairments of air exchangemay result from distention of the abdomen (postoperativelyor due to ascites, obstruction, or a mass) and thoracic trauma(flail chest).
Mixed forms of respiratory failure are common andoccur when disease processes result in more than one pathophysiologic change. Increased secretions seen in asthma often lead to atelectasis and hypoxia, whereasrestrictions of expiratory airflow may lead to hypercarbia.Progression to respiratory failure results from peripheralairway obstruction, extensive atelectasis, and resultant hypoxemia and retention of CO2.
Initial treatment of patients in respiratory distress includes addressing the ABCs (see Chapter 38). Bag/mask ventilationmust be initiated for patients with apnea. In other patients, oxygen therapy is administered using appropriate methods (e.g., simple mask). Administration of oxygen by nasal cannula allows the patient to entrain room air and oxygen, making it an insufficient delivery method for most children in respiratory failure. Delivery methods, including intubation and mechanical ventilation, should be escalated if there is inability to increase oxygen saturation appropriately.