A model analysis of arterial oxygen desaturation during apnea in preterm infants.

Bibliographic Details
Title: A model analysis of arterial oxygen desaturation during apnea in preterm infants.
Authors: Scott A Sands, Bradley A Edwards, Vanessa J Kelly, Malcolm R Davidson, Malcolm H Wilkinson, Philip J Berger
Source: PLoS Computational Biology, Vol 5, Iss 12, p e1000588 (2009)
Publisher Information: Public Library of Science (PLoS), 2009.
Publication Year: 2009
Collection: LCC:Biology (General)
Subject Terms: Biology (General), QH301-705.5
More Details: Rapid arterial O(2) desaturation during apnea in the preterm infant has obvious clinical implications but to date no adequate explanation for why it exists. Understanding the factors influencing the rate of arterial O(2) desaturation during apnea (Sa(O)₂) is complicated by the non-linear O(2) dissociation curve, falling pulmonary O(2) uptake, and by the fact that O(2) desaturation is biphasic, exhibiting a rapid phase (stage 1) followed by a slower phase when severe desaturation develops (stage 2). Using a mathematical model incorporating pulmonary uptake dynamics, we found that elevated metabolic O(2) consumption accelerates Sa(O)₂throughout the entire desaturation process. By contrast, the remaining factors have a restricted temporal influence: low pre-apneic alveolar P(O)₂causes an early onset of desaturation, but thereafter has little impact; reduced lung volume, hemoglobin content or cardiac output, accelerates Sa(O)₂during stage 1, and finally, total blood O(2) capacity (blood volume and hemoglobin content) alone determines Sa(O)₂during stage 2. Preterm infants with elevated metabolic rate, respiratory depression, low lung volume, impaired cardiac reserve, anemia, or hypovolemia, are at risk for rapid and profound apneic hypoxemia. Our insights provide a basic physiological framework that may guide clinical interpretation and design of interventions for preventing sudden apneic hypoxemia.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1553-734X
1553-7358
Relation: http://europepmc.org/articles/PMC2778953?pdf=render; https://doaj.org/toc/1553-734X; https://doaj.org/toc/1553-7358
DOI: 10.1371/journal.pcbi.1000588
Access URL: https://doaj.org/article/cba40a31d3c34e9092ce4024a3bc6b95
Accession Number: edsdoj.ba40a31d3c34e9092ce4024a3bc6b95
Database: Directory of Open Access Journals
More Details
ISSN:1553734X
15537358
DOI:10.1371/journal.pcbi.1000588
Published in:PLoS Computational Biology
Language:English