Document Detail

A model analysis of arterial oxygen desaturation during apnea in preterm infants.
MedLine Citation:
PMID:  19997495     Owner:  NLM     Status:  MEDLINE    
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.
Scott A Sands; Bradley A Edwards; Vanessa J Kelly; Malcolm R Davidson; Malcolm H Wilkinson; Philip J Berger
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Publication Detail:
Type:  Journal Article     Date:  2009-12-04
Journal Detail:
Title:  PLoS computational biology     Volume:  5     ISSN:  1553-7358     ISO Abbreviation:  PLoS Comput. Biol.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-12-09     Completed Date:  2010-02-23     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  101238922     Medline TA:  PLoS Comput Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e1000588     Citation Subset:  IM    
Ritchie Centre for Baby Health Research, Monash Institute of Medical Research, Monash University, Victoria, Australia.
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MeSH Terms
Computational Biology
Hemoglobins / metabolism
Infant, Newborn
Infant, Premature, Diseases / metabolism*
Models, Cardiovascular*
Oxygen / metabolism*
Pulmonary Gas Exchange
Respiratory Physiological Phenomena*
Sleep Apnea, Central / metabolism*
Reg. No./Substance:
0/Hemoglobins; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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