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A neonatal patient with profound anemia may have a normal oxygen saturation level and still be hypoxemic.
To decrease morbidity and mortality, the generally accepted range for peripheral oxygen saturation (SpO2) in a neonate is 88% to 92%.undefined#ref5">5
The goal of oxygen therapy is to deliver sufficient oxygen to the tissues while avoiding hyperoxia and oxygen toxicity. Preterm neonates are especially vulnerable to the effects of hypoxia and hyperoxia.3 Toxic oxygen radicals increase in hyperoxia and in reoxygenation after hypoxemia, resulting in oxidative stress. Oxidative stress is a result of the preterm neonate’s deficiency in the quantity and function of antioxidants that protect the cells from free radicals. Oxidative stress is associated with the development of bronchopulmonary dysplasia and retinopathy of prematurity (ROP).3 Because premature neonates experience intermittent periods of hypoxia and hyperoxia, monitoring the saturations of hemoglobin saturated with oxygen in these patients’ blood is critical.
Pulse oximetry is the most common method of determining arterial oxygen saturation. Circumferential tape probes are wrapped around the neonate’s hand, wrist, foot, or ankle. This pulse oximeter probe contains a light source; a light detector; and a microprocessor, which calculates the differences in the oxygen-rich versus oxygen-poor hemoglobin. Pulse oximetry uses red and infrared light to determine the saturation of hemoglobin bound to oxygen. The oxygen-rich hemoglobin absorbs more of the infrared light, and the hemoglobin without oxygen absorbs more of the red light (Figure 1). The microprocessor calculates the difference between the two and displays a percentage on the monitor. SpO2 is the percentage of the available hemoglobin that carries oxygen.2,5
The acceptable range for SpO2 in neonates is controversial; the generally accepted range is 88% to 92%.3,5 Recommendations for accepting SpO2 between 85% and 95% are also seen in current literature; however, some studies in extremely low-birth-weight neonates have demonstrated that targeting saturation levels less than 90% is associated with lower partial pressure of arterial oxygen (PaO2) levels and higher morbidity.7 The goal is to avoid large variations in saturation levels that have the potential to lead to lung injury and ROP.5 Keeping the SpO2 level between 90% and 92%2 is ideal. In general, oxygen is given for saturations less than 85% and weaned for saturations greater than 95%.4
A neonate’s SpO2 depends on three parameters: the amount and type of hemoglobin present, how well it moves throughout the body, and how easily oxygen binds to and releases from hemoglobin to enter the cells.5
The neonate is unique in that fetal hemoglobin accounts for approximately 80% of the term neonate’s blood volume at birth.7 In utero, the total amount of fetal hemoglobin is gradually replaced with adult hemoglobin starting at 32 weeks’ gestation.7 This gradual replacement continues after birth unless blood transfusions and exchange transfusions hasten the process. Fetal hemoglobin has an increased affinity for oxygen, which results in a pulse oximeter SpO2 reading higher for a given PaO2 than if fetal hemoglobin were not present.
Neonates with decreased hemoglobin concentrations (from anemia or hemorrhage) may have normal SpO2 and still be hypoxemic. Even though the hemoglobin present may be fully saturated, the neonate does not have sufficient hemoglobin to carry enough oxygen to meet the body’s needs.
Neonates with decreased perfusion, from shock, bradycardia, or congenital heart disease, may start with normal SpO2, but because of a decreased blood flow, the hemoglobin is in prolonged contact with cells. The cell’s oxygen demands are increased, the hemoglobin releases oxygen easily, but the blood takes longer to return to the lungs for reoxygenation.
The amount of oxygen bound to the hemoglobin is dependent on the PaO2 to which the hemoglobin is exposed. In the lungs, at the alveolar–capillary interface, the PaO2 is high, and therefore the oxygen binds readily to the hemoglobin. As the blood circulates to other body tissues in which the PaO2 level is lower, the hemoglobin releases the oxygen into the tissue. Specifically, the binding of oxygen to hemoglobin varies with the PaO2. The relationship is nonlinear and forms an S-shaped curve called the oxygen–hemoglobin dissociation curve (ODC). In its simplest form, this curve describes the relation between the PaO2 (x-axis) and the SpO2 (y-axis) (Figure 2). Factors that determine the position of the ODC include temperature, arterial partial pressure of carbon dioxide (PaCO2), and pH.5
A shift to the right in the ODC means the hemoglobin’s affinity for oxygen has decreased and the hemoglobin readily releases oxygen at the cellular level. Factors that move the ODC to the right include physiologic states where tissues need more oxygen, including:5
A shift to the left in the ODC means the hemoglobin’s affinity for oxygen has increased and the hemoglobin is released less readily at the cellular level. Factors that move the ODC to the left include:5
Pulse oximetry readings are altered or not obtainable because of certain conditions:2
Monitoring of a neonate’s SpO2 levels begins at birth in the delivery room. At delivery, the neonate has not transitioned completely away from a fetal circulation pattern with the potential for shunting of blood. Placing the pulse oximeter probe only on the right upper extremity provides a preductal saturation. The preductal saturation accurately reflects the patient’s true status during transition.6 For a neonate at 1 minute old, the SpO2 goal is 60% to 64%, increasing gradually to 85% to 95% by 10 minutes old (Table 1).1
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Rationale: Site selection may affect the accuracy of pulse oximeter readings. In patients with cyanotic heart defect (e.g., coarctation of the aorta, interrupted aortic arch, pulmonary atresia, tetralogy of Fallot) or patent ductus, a preductal saturation is obtained in the right arm, and a postductal saturation is obtained in the left arm or in either foot for more accurate readings.
Avoid sites distal to arterial lines or distal to noninvasive blood pressure cuffs.
Rationale: For an accurate SpO2 measurement, the light source and the photodetector must be directly opposite each other.
Do not apply the probe so tightly that it interrupts blood flow to or from the site. With a tight fit, tissue perfusion may be impaired by circumferential restriction of arterial flow or venous return. Venous congestion may lead to venous pulsations and false readings.
For spot-checking saturations, allow the oximeter several minutes of warmup to average and obtain a reliable saturation reading.
Rationale: Pulse oximetry provides only one piece of data. Physiologic status must be considered to gain a complete assessment of the patient’s condition.
Rationale: Skin probes have the potential to cause medical device–related pressure injuries. Certain conditions (e.g., low perfusion states, use of vasoconstrictive infusions, hypoxia, hypotension, prolonged probe contact, prolonged arterial catheterization in the same extremity as the pulse oximeter probe, hypothermia) may increase the likelihood of injury.
Diaz Kane, M.M. (2022). Pulse oximetry screening for congenital heart defects in the newborn nursery: A review for the general pediatrician. Pediatric Annals, 51(11), e411-e413. doi:10.3928/19382359-20220913-01
Dormishian, A. and others. (2023). Pulse oximetry reliability for detection of hypoxemia under motion in extremely premature infants. Pediatric Research, 93(1), 118-124. doi:10.1038/s41390-022-02258-7
Clinical Review: Marlene L. Bokholdt, MS, RN, CPEN, TCRN
Published: October 2024
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