Oliveira Mayron F, Rodrigues Miguel K, Treptow Erika, Cunha Thúlio M, Ferreira Eloara M V, Neder J Alberto
Pulmonary Function and Clinical Exercise Physiology Unit, Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo, Sao Paulo, Brazil.
Clin Physiol Funct Imaging. 2012 Jan;32(1):52-8. doi: 10.1111/j.1475-097X.2011.01054.x. Epub 2011 Oct 3.
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.
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).
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).
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.
运动期间脑氧合(COx)的变化率(Δ)受血流和动脉血氧含量(CaO₂)影响。目前尚不清楚,对于未达到长期氧疗现行标准但存在运动性低氧血症的慢性阻塞性肺疾病(COPD)患者,(i)运动期间ΔCOx是否会受损,以及(ii)在这一特定亚组人群中,高氧(FIO₂ = 0.4)是否会改善ΔCOx。
共有20名非高碳酸血症男性(FEV₁ = 预计值的47.2 ± 11.5%)在常氧和高氧条件下进行递增式蹬车运动试验,通过近红外光谱法测定ΔCOx(O₂Hb中与无负荷运动相比的倍数变化)。脉搏血氧饱和度测定评估氧合血红蛋白饱和度(SpO₂),阻抗心动图估计心输出量变化(ΔQT)。
与12名“非去饱和者”相比,8名O₂“去饱和者”在常氧下的峰值工作率和ΔCOx较低(P < 0.05)。次最大运动期间ΔCOx的曲线下面积与“去饱和者”的SpO₂下降密切相关(r = 0.92,P < 0.01)。这些患者在高氧下峰值运动能力改善最大(P < 0.05)。尽管主动干预有使次最大ΔQT和平均动脉压降低的趋势,但仅该组的ΔCOx有显著改善(“非去饱和者”和“去饱和者”分别为0.57 ± 0.20和2.09 ± 0.42;P < 0.05)。
运动期间出现去饱和的非低氧血症COPD患者的ΔCOx受损。高氧呼吸能够纠正这些异常,这种效应与CaO₂增加有关,而非中心血流动力学改善。这表明,对于目前无权接受门诊氧疗的COPD患者,补充氧气可改善运动时的COx。