Official reprint from UpToDate®
www.uptodate.com ©2015 UpToDate®

Oxygen monitoring and therapy in the newborn

James M Adams, Jr, MD
Section Editor
Richard Martin, MD
Deputy Editor
Melanie S Kim, MD


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 room 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 100 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 curvilinear 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 hemoglobins".)


Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: Oct 2015. | This topic last updated: Sep 24, 2015.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2015 UpToDate, Inc.
  1. Nunn JF. Nunn's Applied Respiratory Physiology, Butterworth-Heinemann, Oxford 1993. p.282.
  2. Hill JR, Rahimtulla KA. Heat balance and the metabolic rate of new-born babies in relation to environmental temperature; and the effect of age and of weight on basal metabolic rate. J Physiol 1965; 180:239.
  3. Marks KH, Nardis EE, Momin MN. Energy metabolism and substrate utilization in low birth weight neonates under radiant warmers. Pediatrics 1986; 78:465.
  4. Benaron DA, Benitz WE. Maximizing the stability of oxygen delivered via nasal cannula. Arch Pediatr Adolesc Med 1994; 148:294.
  5. Walsh M, Engle W, Laptook A, et al. Oxygen delivery through nasal cannulae to preterm infants: can practice be improved? Pediatrics 2005; 116:857.
  6. Verder H, Albertsen P, Ebbesen F, et al. Nasal continuous positive airway pressure and early surfactant therapy for respiratory distress syndrome in newborns of less than 30 weeks' gestation. Pediatrics 1999; 103:E24.
  7. Van Marter LJ, Allred EN, Pagano M, et al. Do clinical markers of barotrauma and oxygen toxicity explain interhospital variation in rates of chronic lung disease? The Neonatology Committee for the Developmental Network. Pediatrics 2000; 105:1194.
  8. Aly H, Milner JD, Patel K, El-Mohandes AA. Does the experience with the use of nasal continuous positive airway pressure improve over time in extremely low birth weight infants? Pediatrics 2004; 114:697.
  9. Ho JJ, Subramaniam P, Henderson-Smart DJ, Davis PG. Continuous distending pressure for respiratory distress syndrome in preterm infants. Cochrane Database Syst Rev 2002; :CD002271.
  10. Miller MJ, Carlo WA, Martin RJ. Continuous positive airway pressure selectively reduces obstructive apnea in preterm infants. J Pediatr 1985; 106:91.
  11. Stark AR, Goldman MD, Frantz ID 3rd. Lung volume changes, occlusion pressure and chest wall configuration in human infants. Pediatr Res 1979; 13:250.
  12. Davis PG, Henderson-Smart DJ. Nasal continuous positive airways pressure immediately after extubation for preventing morbidity in preterm infants. Cochrane Database Syst Rev 2003; :CD000143.
  13. Buzzella B, Claure N, D'Ugard C, Bancalari E. A randomized controlled trial of two nasal continuous positive airway pressure levels after extubation in preterm infants. J Pediatr 2014; 164:46.
  14. Beker F, Rogerson SR, Hooper SB, et al. The effects of nasal continuous positive airway pressure on cardiac function in premature infants with minimal lung disease: a crossover randomized trial. J Pediatr 2014; 164:726.
  15. Finer NN, Mannino FL. High-flow nasal cannula: a kinder, gentler CPAP? J Pediatr 2009; 154:160.
  16. Shoemaker MT, Pierce MR, Yoder BA, DiGeronimo RJ. High flow nasal cannula versus nasal CPAP for neonatal respiratory disease: a retrospective study. J Perinatol 2007; 27:85.
  17. Collins CL, Barfield C, Horne RS, Davis PG. A comparison of nasal trauma in preterm infants extubated to either heated humidified high-flow nasal cannulae or nasal continuous positive airway pressure. Eur J Pediatr 2014; 173:181.
  18. Dysart K, Miller TL, Wolfson MR, Shaffer TH. Research in high flow therapy: mechanisms of action. Respir Med 2009; 103:1400.
  19. Frizzola M, Miller TL, Rodriguez ME, et al. High-flow nasal cannula: impact on oxygenation and ventilation in an acute lung injury model. Pediatr Pulmonol 2011; 46:67.
  20. Kotecha SJ, Adappa R, Gupta N, et al. Safety and Efficacy of High-Flow Nasal Cannula Therapy in Preterm Infants: A Meta-analysis. Pediatrics 2015; 136:542.
  21. Williams AJ. ABC of oxygen: assessing and interpreting arterial blood gases and acid-base balance. BMJ 1998; 317:1213.
  22. Harsten A, Berg B, Inerot S, Muth L. Importance of correct handling of samples for the results of blood gas analysis. Acta Anaesthesiol Scand 1988; 32:365.
  23. Hansen JE, Simmons DH. A systematic error in the determination of blood PCO2. Am Rev Respir Dis 1977; 115:1061.
  24. Neff TA. Routine oximetry. A fifth vital sign? Chest 1988; 94:227.
  25. Hay WW Jr, Brockway JM, Eyzaguirre M. Neonatal pulse oximetry: accuracy and reliability. Pediatrics 1989; 83:717.
  26. Durand M, Ramanathan R. Pulse oximetry for continuous oxygen monitoring in sick newborn infants. J Pediatr 1986; 109:1052.
  27. Levesque BM, Pollack P, Griffin BE, Nielsen HC. Pulse oximetry: what's normal in the newborn nursery? Pediatr Pulmonol 2000; 30:406.
  28. Brockmann PE, Poets A, Urschitz MS, et al. Reference values for pulse oximetry recordings in healthy term neonates during their first 5 days of life. Arch Dis Child Fetal Neonatal Ed 2011; 96:F335.
  29. Harigopal S, Satish HP, Taktak AF, et al. Oxygen saturation profile in healthy preterm infants. Arch Dis Child Fetal Neonatal Ed 2011; 96:F339.
  30. Hagadorn JI, Furey AM, Nghiem TH, et al. Achieved versus intended pulse oximeter saturation in infants born less than 28 weeks' gestation: the AVIOx study. Pediatrics 2006; 118:1574.
  31. Clucas L, Doyle LW, Dawson J, et al. Compliance with alarm limits for pulse oximetry in very preterm infants. Pediatrics 2007; 119:1056.
  32. Greenspan JS, Goldsmith JP. Oxygen therapy in preterm infants: hitting the target. Pediatrics 2006; 118:1740.
  33. Poets CF, Southall DP. Noninvasive monitoring of oxygenation in infants and children: practical considerations and areas of concern. Pediatrics 1994; 93:737.
  34. Vagedes J, Poets CF, Dietz K. Averaging time, desaturation level, duration and extent. Arch Dis Child Fetal Neonatal Ed 2013; 98:F265.
  35. Jennis MS, Peabody JL. Pulse oximetry: an alternative method for the assessment of oxygenation in newborn infants. Pediatrics 1987; 79:524.
  36. Dawson JA, Kamlin CO, Vento M, et al. Defining the reference range for oxygen saturation for infants after birth. Pediatrics 2010; 125:e1340.
  37. Quine D, Stenson BJ. Arterial oxygen tension (Pao2) values in infants <29 weeks of gestation at currently targeted saturations. Arch Dis Child Fetal Neonatal Ed 2009; 94:F51.
  38. Castillo A, Sola A, Baquero H, et al. Pulse oxygen saturation levels and arterial oxygen tension values in newborns receiving oxygen therapy in the neonatal intensive care unit: is 85% to 93% an acceptable range? Pediatrics 2008; 121:882.
  39. Supplemental Therapeutic Oxygen for Prethreshold Retinopathy Of Prematurity (STOP-ROP), a randomized, controlled trial. I: primary outcomes. Pediatrics 2000; 105:295.
  40. SUPPORT Study Group of the Eunice Kennedy Shriver NICHD Neonatal Research Network, Carlo WA, Finer NN, et al. Target ranges of oxygen saturation in extremely preterm infants. N Engl J Med 2010; 362:1959.
  41. Schmidt B, Whyte RK, Asztalos EV, et al. Effects of targeting higher vs lower arterial oxygen saturations on death or disability in extremely preterm infants: a randomized clinical trial. JAMA 2013; 309:2111.
  42. BOOST II United Kingdom Collaborative Group, BOOST II Australia Collaborative Group, BOOST II New Zealand Collaborative Group, et al. Oxygen saturation and outcomes in preterm infants. N Engl J Med 2013; 368:2094.
  43. Manja V, Lakshminrusimha S, Cook DJ. Oxygen saturation target range for extremely preterm infants: a systematic review and meta-analysis. JAMA Pediatr 2015; 169:332.
  44. Poets CF, Roberts RS, Schmidt B, et al. Association Between Intermittent Hypoxemia or Bradycardia and Late Death or Disability in Extremely Preterm Infants. JAMA 2015; 314:595.
  45. Bancalari E, Claure N. Oxygenation targets and outcomes in premature infants. JAMA 2013; 309:2161.
  46. Polin RA, Bateman D. Oxygen-saturation targets in preterm infants. N Engl J Med 2013; 368:2141.
  47. Lim K, Wheeler KI, Gale TJ, et al. Oxygen saturation targeting in preterm infants receiving continuous positive airway pressure. J Pediatr 2014; 164:730.
  48. Claure N, D'Ugard C, Bancalari E. Automated adjustment of inspired oxygen in preterm infants with frequent fluctuations in oxygenation: a pilot clinical trial. J Pediatr 2009; 155:640.
  49. Hallenberger A, Poets CF, Horn W, et al. Closed-loop automatic oxygen control (CLAC) in preterm infants: a randomized controlled trial. Pediatrics 2014; 133:e379.