Children have anatomic and physiologic differences that should be considered when evaluating a pediatric patient presenting in respiratory distress. Young infants may be obligate nose breathers, and any degree of obstruction of the nasal passages can produce respiratory difficulty.

The chest wall of children is more flexible and the muscles are less developed compared to adults. The diaphragm is more prone to fatigue. The limitation of diaphragmatic movement by gastric distention, and increased residual capacity from air trapping from asthma, bronchiolitis, or foreign body obstruction can result in reduction of tidal volume, which may produce respiratory failure. The relatively smaller lower airways are especially vulnerable to mucus plugging and ventilation–perfusion mismatch associated with common diseases of the lower airways, such as asthma and bronchiolitis.^1,2

The actual area available for gas exchange in infants and young children is relatively limited. Alveolar space doubles by 18 months of age and triples by 3 years of age. The limited ability to recruit additional alveoli makes the infant dependent on increasing the respiratory rate to augment minute ventilation and eliminate carbon dioxide. Tachypnea is therefore a universal finding in infants and young children in respiratory distress.¹ The combination of increased muscle exertion and the need to sustain a rapid respiratory rate can result in progressive muscle fatigue and respiratory failure. This is especially true in young infants, who have a limited metabolic reserve. Children have about twice the oxygen consumption as adults,¹ and they have proportionally smaller functional residual capacity. Infants and children have the potential to desaturate more quickly than adults^1,3 (see Chapter 18 for airway differences between infants and children).

Most commonly, a patient in respiratory distress will present to the ED with a history of difficulty breathing. Parents may note coughing, rapid noisy breathing, or a change in behavior. Feeding problems are often a sign of respiratory compromise in infants. In older children, wheezing or decreased physical activity may be presenting complaints.

The past medical history is essential in determining the etiology of the acute problem. Infants with a history of significant prematurity may have bronchopulmonary dysplasia, a chronic lung disease syndrome characterized by varying degrees of hypoxia, hypercarbia, reactive airway disease, and a heightened susceptibility to respiratory infections. Infants with a history of sweating during bottle feedings may have undiagnosed congestive heart failure. For patients with a history of asthma, information regarding the frequency and severity of past exacerbations is important in determining both the acute treatment and disposition. A patient with a history of a chronic cough or recurrent pneumonia may have an underlying lung disorder, such as reactive airway disease, cystic fibrosis, a retained foreign body, or an undiagnosed lung anomaly. Respiratory symptoms can also be caused by systemic disorders. Effortless tachypnea and hyperpnea accompany disorders such as diabetic ketoacidosis and sepsis, as an attempt to compensate for metabolic acidosis.^2,4

Simply observing the patient yields a wealth of information regarding the degree of respiratory distress. Infants and young children with mild respiratory difficulty will have normal mental status. Patients with more severe disease become irritable or anxious and can appear restless and unable to assume a comfortable position. Children in extreme distress are usually unable to lie supine and may exhibit head-bobbing. Young infants in severe distress will appear anxious, will often not make eye contact, and usually will not smile. If feeding is attempted, they will refuse the bottle, since the work of breathing precludes the exertion of sucking. Respiratory failure is heralded by extreme agitation followed by lethargy or somnolence. Cyanosis is an ominous finding.^1,2

Observing the patient’s chest will add to the assessment of the degree of respiratory distress. Patients with significant respiratory distress will virtually always be tachypneic unless they are about to arrest. Because respiratory rate is age dependent and can be influenced by underlying medical conditions, it must be viewed in the context of the overall clinical picture. Visual inspection of the chest wall may reveal retractions, which signify the use of accessory muscles of respiration. Retractions can be seen in the supraclavicular and subcostal areas as well. In more severe cases, nasal flaring is seen. Retractions imply a significant degree of respiratory distress and should not be overlooked.^1,2

Listening to audible breath sounds will help to localize the pathology. Stridor is generally heard on inspiration, but with severe obstruction, it can be present on both inspiration and exhalation. Stridor suggests upper airway pathology, such as croup, epiglottitis, laryngomalacia, or foreign body obstruction. Grossly audible wheezing usually indicates obstruction of the lower airways. Lower airway disease resulting in alveolar collapse can also be associated with grunting, which is caused by premature closure of the glottis during exhalation. Grunting increases airway pressure and can help prevent further alveolar collapse and thus preserve functional residual capacity. Grunting is most often seen in infants and always indicates severe respiratory distress, whether from primary lung disease or a systemic illness, such as sepsis.^1,2,4

Auscultation of the chest supplements the information gained from observation of the patient. The first factor to assess is air exchange. Upper airway obstruction predominantly affects the inhalation of air, whereas lower airway obstruction predominantly affects exhalation. Patients who appear to be struggling to breathe and have limited air exchange appreciated on auscultation are at high risk for respiratory failure.

Pulse oximetry is especially useful in infants, in whom the physical findings may be difficult to assess and an arterial blood gas difficult to obtain. The pulse oximeter does not measure the arterial carbon dioxide tension (PaCO₂) or acid–base status, and therefore careful clinical correlation is necessary in many situations, such as asthma and bronchiolitis, in which CO₂ retention and respiratory acidosis are early markers of respiratory failure. Pulse oximetry is also unreliable for patients with low-perfusion states, carbon monoxide poisoning, and methemoglobinemia.²

Respiratory failure is often defined as arterial oxygen tension (PaO₂) <60 mmHg despite supplemental inhaled oxygen of 60% or PaCO₂ >60 mmHg. The clinical equivalent of this is the failure to achieve a high oxygen saturation by pulse oximetry despite supplemental oxygen. A high PaCO₂ can be suspected when there is poor air exchange on auscultation. End-tidal PCO₂ (EtCO₂) can provide real-time estimates of the PaCO₂ in most instances.^1,2

Absolute values of arterial oxygen and carbon dioxide tension must be viewed in the context of the clinical situation as well as the patient’s baseline pulmonary status. Some patients with chronic lung disease might have a baseline PaCO₂ of 50 mmHg or more.² A patient may not meet strict criteria for respiratory failure but may develop muscle fatigue such that the work of breathing cannot be sustained despite blood gas values that appear adequate. In most children with severe lung disease, parents are aware of baseline information that can aid the physician in interpreting oxygen saturation and blood gas values. Another caveat is that respiratory failure and resuscitative efforts can evolve rapidly such that a blood gas value 3 minutes ago might be irrelevant if the patient has worsened or substantially improved during those 3 minutes.