Effects of oxygen supplementation on cerebral oxygenation during exercise in chronic obstructive pulmonary disease patients not entitled to long-term oxygen therapy.

Clin Physiol Funct Imaging

Pulmonary Function and Clinical Exercise Physiology Unit, Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo, Sao Paulo, Brazil.

Published: January 2012

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.

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Source
http://dx.doi.org/10.1111/j.1475-097X.2011.01054.xDOI Listing

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