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Effects of oxygen supplementation on cerebral oxygenation during exercise in chronic obstructive pulmonary disease patients not entitled to long‐term oxygen therapy
Author(s) -
Oliveira Mayron F.,
Rodrigues Miguel K.,
Treptow Erika,
Cunha Thúlio M.,
Ferreira Eloara M. V.,
Neder J Alberto
Publication year - 2012
Publication title -
clinical physiology and functional imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.608
H-Index - 67
eISSN - 1475-097X
pISSN - 1475-0961
DOI - 10.1111/j.1475-097x.2011.01054.x
Subject(s) - medicine , hyperoxia , copd , oxygenation , impedance cardiography , cardiology , hypoxemia , population , oxygen saturation , anesthesia , heart rate , pulse oximetry , blood pressure , oxygen , lung , stroke volume , chemistry , organic chemistry , environmental health
Summary Background: The rate of change (Δ) in cerebral oxygenation (COx) during exercise is influenced by blood flow and arterial O 2 content (CaO 2 ). It is currently unclear whether ΔCOx would (i) be impaired during exercise in patients with chronic obstructive pulmonary disease (COPD) who do not fulfil the current criteria for long‐term O 2 therapy but present with exercise‐induced hypoxaemia and (ii) improve with hyperoxia (FIO 2 = 0·4) in this specific sub‐population. Methods: A total of 20 non‐hypercapnic men (FEV 1 = 47·2 ± 11·5% pred) underwent incremental cycle ergometer exercise tests under normoxia and hyperoxia with ΔCOx (fold‐changes from unloaded exercise in O 2 Hb) being determined by near‐infrared spectroscopy. Pulse oximetry assessed oxyhaemoglobin saturation (SpO 2 ), and impedance cardiography estimated changes in cardiac output (ΔQT). Results: Peak work rate and ΔCOx in normoxia were lower in eight O 2 ‘desaturators’ compared with 12 ‘non‐desaturators’ ( P <0·05). Area under ΔCOx during sub‐maximal exercise was closely related to SpO 2 decrements in ‘desaturators’ ( r = 0·92, P <0·01). These patients showed the largest improvement in peak exercise capacity with hyperoxia ( P <0·05). Despite a trend to lower sub‐maximal ΔQT and mean arterial pressure with active intervention, ΔCOx was significantly improved only in this group (0·57 ± 0·20 versus 2·09 ± 0·42 for ‘non‐desaturators’ and ‘desaturators’, respectively; P <0·05). Conclusions: ΔCOx was impaired in non‐hypoxaemic patients with COPD who desaturated during exercise. Hyperoxic breathing was able to correct for these abnormalities, an effect related to enhanced CaO 2 rather than improved central haemodynamics. This indicates that O 2 supplementation ameliorates exercise COx in patients with COPD who are not currently entitled to ambulatory O 2 therapy.