OBJECTIVES: Increasing PaO2 can increase brain tissue PO2 (PbtO2). Nevertheless, the small increase in arterial O2 content induced by hyperoxia does not increase O2 delivery much, especially when cerebral blood flow (CBF) is low, and the effectiveness of hyperoxia as a therapeutic intervention remains controversial. The purpose of this study was to examine the role of regional (r)CBF at the site of the PO2 probe in determining the response of PbtO2 to induced hyperoxia. METHODS: The authors measured PaO2 and PbtO2 at baseline normoxic conditions and after increasing inspired O2 concentration to 100% on 111 occasions in 83 patients with severe traumatic brain injury in whom a stable xenon-enhanced computed tomography measurement of CBF was available. The O2 reactivity was calculated as the change in PbtO2 x 100/change in PaO2. RESULTS: The O2 reactivity was significantly different (p < 0.001) at the 5 levels of rCBF (<10, 11-15, 16-20, 21-40, and > 40 ml/100 g/min). When rCBF was < 20 ml/100 g/min, the increase in PbtO2 induced by hyperoxia was very small compared with the increase that occurred when rCBF was > 20 ml/100 g/min. CONCLUSIONS: Although the level of CBF is probably only one of the factors that determines the PbtO2 response to hyperoxia, it is apparent from these results that the areas of the brain that would most likely benefit from improved oxygenation are the areas that are the least likely to have increased PbtO2.
OBJECTIVES: Increasing PaO2 can increase brain tissue PO2 (PbtO2). Nevertheless, the small increase in arterial O2 content induced by hyperoxia does not increase O2 delivery much, especially when cerebral blood flow (CBF) is low, and the effectiveness of hyperoxia as a therapeutic intervention remains controversial. The purpose of this study was to examine the role of regional (r)CBF at the site of the PO2 probe in determining the response of PbtO2 to induced hyperoxia. METHODS: The authors measured PaO2 and PbtO2 at baseline normoxic conditions and after increasing inspired O2 concentration to 100% on 111 occasions in 83 patients with severe traumatic brain injury in whom a stable xenon-enhanced computed tomography measurement of CBF was available. The O2 reactivity was calculated as the change in PbtO2 x 100/change in PaO2. RESULTS: The O2 reactivity was significantly different (p < 0.001) at the 5 levels of rCBF (<10, 11-15, 16-20, 21-40, and > 40 ml/100 g/min). When rCBF was < 20 ml/100 g/min, the increase in PbtO2 induced by hyperoxia was very small compared with the increase that occurred when rCBF was > 20 ml/100 g/min. CONCLUSIONS: Although the level of CBF is probably only one of the factors that determines the PbtO2 response to hyperoxia, it is apparent from these results that the areas of the brain that would most likely benefit from improved oxygenation are the areas that are the least likely to have increased PbtO2.
Authors: Anthony A Figaji; Eugene Zwane; Crispin Thompson; A Graham Fieggen; Andrew C Argent; Peter D Le Roux; Jonathan C Peter Journal: Childs Nerv Syst Date: 2009-02-13 Impact factor: 1.475
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Authors: Paul Kaloostian; Claudia Robertson; Shankar P Gopinath; Martina Stippler; C Christopher King; Clifford Qualls; Howard Yonas; Edwin M Nemoto Journal: J Neurotrauma Date: 2012-03-20 Impact factor: 5.269
Authors: Anthony A Figaji; Eugene Zwane; A Graham Fieggen; Andrew C Argent; Peter D Le Roux; Jonathan C Peter Journal: Neurocrit Care Date: 2010-06 Impact factor: 3.210
Authors: C A C Wijman; S M Smirnakis; P Vespa; K Szigeti; W C Ziai; M M Ning; J Rosand; D F Hanley; R Geocadin; C Hall; P D Le Roux; J I Suarez; O O Zaidat Journal: Neurocrit Care Date: 2012-02 Impact factor: 3.210
Authors: Anthony A Figaji; Eugene Zwane; Crispin Thompson; A Graham Fieggen; Andrew C Argent; Peter D Le Roux; Jonathan C Peter Journal: Childs Nerv Syst Date: 2009-02-13 Impact factor: 1.475