Fetal hemoglobin predominates in the neonate and young infant, and this causes another important difference in respiratory physiology from the older child and adult. The oxyhemoglobin dissociation curve is shifted to the left in neonates because of fetal hemoglobin, meaning that the partial pressure of oxygen necessary to produce an oxyhemoglobin saturation of 50 % (the P₅₀) is only 19 mmHg, versus 27 mmHg with mature adult hemoglobin A [6] (Fig. 8.2). This is an adaptation to fetal life, where oxygen tensions are low, and with hemoglobin F loading the hemoglobin with oxygen molecules is facilitated; however, unloading of oxygen to the tissues is more difficult with a left-shifted curve. Therefore in the neonate and young infant, a given oxygen tension will produce a higher oxygen saturation, but this extra reserve is required to provide additional oxygen to unload to the tissues. Adult hemoglobin A predominates by 6 months of age.

Pulse oximetry is the standard for monitoring of oxygenation during all sedation procedures. (Refer to Chaps. 2 and 6.) Pulse oximeter arterial saturation (SpO₂) is a very useful monitor, generally accurate to ±2 % when compared to arterial blood oxygen saturation measured by co-oximetry. In a child without cardiac or pulmonary disease, normal SpO₂ is 96–100 % on room air and unsedated. Sedative medications often cause a degree of hypoventilation, both in slowing respiratory rate, and decreasing tidal volumes and FRC. Upper airway obstruction is also common, which may interfere with oxygenation. These factors make it necessary to deliver supplemental oxygen to virtually all patients undergoing sedation procedures, either by nasal cannula or face mask, to enable SpO₂ to remain in the normal 96–100 % range. A decrease of 5 % or less from baseline, as long as the patient is otherwise stable without significant respiratory depression or upper airway obstruction, is common and can usually be treated with increased supplemental oxygen. A decrease of 10 % or more from baseline is cause for urgent intervention to detect and treat upper airway obstruction or hypoventilation—the two most common causes of arterial desaturation during sedation. Children with cyanotic congenital heart disease may have resting awake SpO₂ ranging from 70 to 95 %, and it is important to understand the anatomy, pathophysiology, and normal baseline saturations before proceeding with sedation in these patients. The general guidelines of a 5 % decrease from baseline being common and treated with additional supplemental oxygen, and a 10 % decrease, a cause for urgent intervention, are applicable to this population as well. Other patients with chronic lung diseases—i.e., bronchopulmonary dysplasia (BPD) or cystic fibrosis—may also have decreased baseline SpO₂, often ranging from 85 to 95 %.

Monitoring of respiration also often includes end-tidal CO₂, which can easily be monitored using a special or modified nasal cannula. Although dilution of the exhaled gas with inspired oxygen, poor fit of nasal cannula, increased dead space ventilation, or right to left intracardiac shunting often increases the gap between arterial blood PaCO₂ and end-tidal CO₂, it is a very sensitive monitor of airway obstruction, and an accurate method to measure respiratory rate. In addition, low cardiac output states or cardiac arrest is accompanied by a sudden decrease or absence of end-tidal CO₂.

Common conditions in pediatric patients that reduce respiratory reserve even further include BPD in former premature infants who suffered from respiratory distress syndrome (RDS) [7]. BPD is defined as a chronic condition of fibrosis and loss of alveoli in the lung following RDS with a requirement for supplemental oxygen beyond 30 days of life. These infants may present for sedation months or years later, and even though they have apparently recovered, pulmonary reserve is often considerably limited. Other common chronic conditions include asthma or reactive airway disease, affecting an estimated six million children in the USA [8]. Pre-sedation assessment must always include questioning about asthma and a thorough airway and pulmonary examination; elective sedation in the face of an asthma exacerbation is contraindicated.

Children also have frequent upper respiratory infections (URIs), which predispose them to increased airway complications during a sedation procedure. Elective sedation procedures should be performed in children with URIs only after a thorough risk–benefit assessment.

All of the factors reviewed earlier make the small infant in particular vulnerable to rapid onset of hypoxemia and hypercarbia if sedated too deeply, and the practitioner must be vigilant especially when sedating infants. Supplemental oxygen should be used in almost every setting in which infants and children are sedated, the only exceptions being in premature neonates where retinopathy of prematurity may be a risk, and in relatively uncommon congenital heart defects in neonates with a single functional ventricle, such as hypoplastic left heart syndrome.