Target Oxygen Levels and Critical Care of the Newborn

Author(s): Joseph J. Vettukattil*

Journal Name: Current Pediatric Reviews

Volume 16 , Issue 1 , 2020

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Abstract:

Despite our growing experience in the medical care of extremely preterm infants and critically ill neonates, there are serious gaps in the understanding and clinical application of the adaptive physiology of the newborn. Neonatal physiology is often misinterpreted and considered similar to that of adult physiology. The human psyche has been seriously influenced, both from an evolutionary and survival point of view, by the cause and effect of hypoxemia which is considered as a warning sign of impending death. Within this context, it is unimaginable for even the highly trained professionals to consider saturation as low as 65% as acceptable. However, all available data suggests that newborns can thrive in a hypoxemic environment as they are conditioned to withstand extreme low saturations in the fetal environment. An approach utilizing the benefits of the hypoxic conditioning would prompt the practice of optimal targeted oxygen saturation range in the clinical management of the newborn. Our current understanding of cyanotic congenital heart disease and the physiology of single ventricle circulation, where oxygen saturation in mid 70s is acceptable, is supported by clinical and animal studies. This article argues the need to challenge our current acceptable target oxygen saturation in the newborn and provides the reasoning behind accepting lower target oxygen levels in the critically ill newborn. Challenging the current practice is expected to open a debate paving the way to understand the risks of high target oxygen levels in the newborn compared with the benefits of permissive hypoxia in avoiding the associated morbidity and mortality of oxygen radical injury.

Keywords: Cyanotic congenital heart disease, hypoxic preconditioning, hypoxemic hypoxic preconditioning, ischemic preconditioning, primary hypoxic preconditioning, critical care.

[1]
Verges S, Chacaroun S, Godin-Ribuot D, Baillieul S. Hypoxic conditioning as a new therapeutic modality. Front Pediatr 2015; 3: 58.
[http://dx.doi.org/10.3389/fped.2015.00058] [PMID: 26157787]
[2]
Hutter D, Kingdom J, Jaeggi E. Causes and mechanisms of intrauterine hypoxia and its impact on the fetal cardiovascular system: a review. Int J Pediatr 2010; 2010401323
[http://dx.doi.org/10.1155/2010/401323] [PMID: 20981293]
[3]
Patterson AJ, Zhang L. Hypoxia and fetal heart development. Curr Mol Med 2010; 10(7): 653-66.
[http://dx.doi.org/10.2174/156652410792630643] [PMID: 20712587]
[4]
Vento M, Teramo K. Evaluating the fetus at risk for cardiopulmonary compromise. Semin Fetal Neonatal Med 2013; 18(6): 324-9.
[http://dx.doi.org/10.1016/j.siny.2013.08.003] [PMID: 24055407]
[5]
James JL, Stone PR, Chamley LW. The regulation of trophoblast differentiation by oxygen in the first trimester of pregnancy. Hum Reprod Update 2006; 12(2): 137-44.
[http://dx.doi.org/10.1093/humupd/dmi043] [PMID: 16234296]
[6]
Compernolle V, Brusselmans K, Franco D, et al. Cardia bifida, defective heart development and abnormal neural crest migration in embryos lacking hypoxia-inducible factor-1alpha. Cardiovasc Res 2003; 60(3): 569-79.
[http://dx.doi.org/10.1016/j.cardiores.2003.07.003] [PMID: 14659802]
[7]
Meyer K, Lubo Zhang . Fetal programming of cardiac function and disease. Reprod Sci 2007; 14(3): 209-16.
[http://dx.doi.org/10.1177/1933719107302324] [PMID: 17636233]
[8]
Saugstad OD. Oxygen toxicity in the neonatal period. Acta Paediatr Scand 1990; 79(10): 881-92.
[http://dx.doi.org/10.1111/j.1651-2227.1990.tb11348.x] [PMID: 2264459]
[9]
Tin W, Milligan DW, Pennefather P, Hey E. Pulse oximetry, severe retinopathy, and outcome at one year in babies of less than 28 weeks gestation. Arch Dis Child Fetal Neonatal Ed 2001; 84(2): F106-10.
[http://dx.doi.org/10.1136/fn.84.2.F106] [PMID: 11207226]
[10]
Marino BS, Lipkin PH, Newburger JW, et al. American Heart Association Congenital Heart Defects Committee, Council on Cardiovascular Disease in the Young, Council on Cardiovascular Nursing, and Stroke Council. Neurodevelopmental outcomes in children with congenital heart disease: evaluation and management: a scientific statement from the American Heart Association. Circulation 2012; 126(9): 1143-72.
[http://dx.doi.org/10.1161/CIR.0b013e318265ee8a] [PMID: 22851541]
[11]
Bernhardt WM, Warnecke C, Willam C, Tanaka T, Wiesener MS, Eckardt KU. Organ protection by hypoxia and hypoxia-inducible factors. Methods Enzymol 2007; 435: 221-45.
[http://dx.doi.org/10.1016/S0076-6879(07)35012-X] [PMID: 17998057]
[12]
Faeh D, Gutzwiller F, Bopp M. Swiss National Cohort Study Group. Lower mortality from coronary heart disease and stroke at higher altitudes in Switzerland. Circulation 2009; 120(6): 495-501.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.108.819250] [PMID: 19635973]
[13]
Guppy M, Withers P. Metabolic depression in animals: physiological perspectives and biochemical generalizations. Biol Rev Camb Philos Soc 1999; 74(1): 1-40.
[http://dx.doi.org/10.1017/S0006323198005258] [PMID: 10396183]
[14]
Semenza GL. Regulation of mammalian O2 homeostasis by hypoxia-inducible factor 1. Annu Rev Cell Dev Biol 1999; 15: 551-78.
[http://dx.doi.org/10.1146/annurev.cellbio.15.1.551] [PMID: 10611972]
[15]
Lemus-Varela ML, Flores-Soto ME, Cervantes-Munguía R, et al. Expression of HIF-1 alpha, VEGF and EPO in peripheral blood from patients with two cardiac abnormalities associated with hypoxia. Clin Biochem 2010; 43(3): 234-9.
[16]
Bigham AW, F.S Lee. Human high-altitude adaptation: forward genetics meets the HIF pathway. Genes Dev 2014; 28(20): 2189-204.
[PMID: 25319824]
[17]
Beall CM, Cavalleri GL, Deng L, et al. Natural selection on EPAS1 (HIF2alpha) associated with low hemoglobin concentration in Tibetan highlanders. Proc Natl Acad Sci USA 2010; 107(25): 11459-64.
[http://dx.doi.org/10.1073/pnas.1002443107] [PMID: 20534544]
[18]
Simonson TS, Yang Y, Huff CD, et al. Genetic evidence for high-altitude adaptation in Tibet. Science 2010; 329(5987): 72-5.
[http://dx.doi.org/10.1126/science.1189406] [PMID: 20466884]
[19]
Yi X, Liang Y, Huerta-Sanchez E, et al. Sequencing of 50 human exomes reveals adaptation to high altitude. Science 2010; 329(5987): 75-8.
[http://dx.doi.org/10.1126/science.1190371] [PMID: 20595611]
[20]
Song D, Li LS, Arsenault PR, et al. Defective Tibetan PHD2 binding to p23 links high altitude adaption to altered oxygen sensing. J Biol Chem 2014; 289(21): 14656-65.
[http://dx.doi.org/10.1074/jbc.M113.541227] [PMID: 24711448]
[21]
Wang D, Liu YL, Lü XD, et al. Lung microRNA profile in chronic cyanotic piglets with decreased pulmonary blood flow. Chin Med J (Engl) 2013; 126(12): 2260-4.
[PMID: 23786935]
[22]
Brunken RC, Perloff JK, Czernin J, et al. Myocardial perfusion reserve in adults with cyanotic congenital heart disease. Am J Physiol Heart Circ Physiol 2005; 289(5): H1798-806.
[http://dx.doi.org/10.1152/ajpheart.01309.2004] [PMID: 16006539]
[23]
Perloff JK, Urschell CW, Roberts WC, Caulfield WH Jr. Aneurysmal ilatation of the coronary arteries in cyanotic congenital cardiac disease. Report of a forty year old patient with the Taussig-Bing complex. Am J Med 1968; 45(5): 802-10.
[http://dx.doi.org/10.1016/0002-9343(68)90214-3] [PMID: 5687261]
[24]
Dedkov EI, Perloff JK, Tomanek RJ, Fishbein MC, Gutterman DD. The coronary microcirculation in cyanotic congenital heart disease. Circulation 2006; 114(3): 196-200.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.105.602771] [PMID: 16831984]


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Article Details

VOLUME: 16
ISSUE: 1
Year: 2020
Page: [2 - 5]
Pages: 4
DOI: 10.2174/1573396315666191016094828

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