Oxygen supplementation is an important component of intensive care of the newborn. Careful monitoring is required to minimize pulmonary toxicity or the consequences of hypoxemia or hyperoxia. The two main complications of excessive oxygen are lung injury and retinopathy of prematurity. They are caused by different factors, from lung injury associated with high inspired oxygen concentration, and retinopathy associated with high arterial oxygen tension (see "Retinopathy of prematurity"). On the other hand, there are concerns that excessively low oxygen saturation may be associated with increased mortality or risk of neurodevelopmental impairment.
Oxygen administration, monitoring, and target levels for the neonate, including the premature infant, will be reviewed here. Oxygen administration during neonatal resuscitation in the delivery is discussed separately. (See "Neonatal resuscitation in the delivery room", section on 'Supplemental oxygen'.)
Normal cellular function depends upon a continuous supply of oxygen. Inhaled oxygen diffuses across the alveolar-capillary membrane and into the pulmonary capillary blood. The partial pressure for oxygen in the alveoli (approximately 150 mmHg breathing room air at sea level) is greater than in mixed venous blood (40 mmHg) and in the mitochondria (<10 mmHg). This gradient maintains the arterial oxygen tension (PaO2) and is largely the driving force for oxygen delivery to cells.
Oxygen diffuses into the blood where it is predominantly bound to hemoglobin in red blood cells, with a small proportion being dissolved in plasma. The relationship between PaO2 and hemoglobin is described by the S-shaped oxyhemoglobin dissociation curve (figure 1). At a PaO2 above 90 mmHg, the curve is nearly flat, and hemoglobin is almost completely saturated. At lower values of PaO2, the curve falls steeply, promoting release of oxygen to the tissues.
Oxygen affinity, which refers to the ability of hemoglobin to bind or release oxygen, is modulated by pH, CO2 (in part independent of pH), 2,3-diphosphoglycerate (DPG), temperature, and fetal hemoglobin (figure 1). Lower pH, higher CO2, increased temperature, and a decreased proportion of fetal hemoglobin reduce oxygen affinity. These shifts in affinity promote oxygen uptake in the pulmonary capillaries and release into the tissues. (See "Structure and function of normal human hemoglobins".)