Smith R P, Johnson M K, Ashley J, Rudkin S T, White R J
Department of Medicine, Frenchay Hospital, Bristol, UK.
Thorax. 1998 Jul;53(7):572-6. doi: 10.1136/thx.53.7.572.
Exercise training is being promoted increasingly for patients with chronic obstructive pulmonary disease (COPD). Many of these patients experience exercise related arterial desaturation but the clinical importance of these hypoxaemic episodes is not known. QTc dispersion is a marker of myocardial repolarisation abnormalities and there has been much interest in its role as a non-invasive predictor of cardiac arrhythmias and sudden death. However, little is known about the dynamic effects that exercise and hypoxaemia have on QTc dispersion in patients with COPD.
20 patients with severe COPD (FEV1 < 40% predicted) undertook two 15 minute treadmill tests at a speed calculated to produce a constant workload of 50% maximum oxygen consumption (VO2max) during which they were blindly given either air or 35% oxygen in random order. Physiological measurements taken throughout exercise included 12 lead electrocardiograms from which QTc dispersion values were calculated according to standard criteria. Nine of the patients who desaturated with exercise were studied further. A similar degree of hypoxaemia was induced at rest by giving them a titrated mixture of air and oxygen and the changes in QTc dispersion were recorded.
11 of the 20 patients developed significant hypoxaemia (desaturation by > or = 5% to < 90%) with exercise breathing air. There were no significant changes in QTc dispersion with either exercise or hypoxaemia. There were no significant changes in QTc dispersion when comparing those who did and did not desaturate, and those with and without a high baseline QTc dispersion values (60 ms). Induced hypoxaemia without exercise also failed to worsen QTc dispersion.
No evidence was found to suggest that exercise, even when associated with hypoxaemia, causes myocardial repolarisation abnormalities in patients with COPD.
慢性阻塞性肺疾病（COPD）患者越来越多地接受运动训练。这些患者中有许多人在运动时会出现与运动相关的动脉血氧饱和度下降，但这些低氧血症发作的临床重要性尚不清楚。QTc离散度是心肌复极异常的一个指标，人们对其作为心律失常和猝死的非侵入性预测指标的作用非常感兴趣。然而，关于运动和低氧血症对COPD患者QTc离散度的动态影响知之甚少。
20例重度COPD患者（FEV1<预计值的40%）进行了两次15分钟的跑步机测试，速度设定为产生相当于最大耗氧量（VO2max）50%的恒定工作量，在此期间，他们被随机顺序盲目给予空气或35%氧气。运动过程中进行的生理测量包括12导联心电图，根据标准标准计算QTc离散度值。对9例运动时出现血氧饱和度下降的患者进行了进一步研究。通过给予他们空气和氧气的滴定混合物在休息时诱导出相似程度的低氧血症，并记录QTc离散度的变化。
20例患者中有11例在运动时呼吸空气出现明显低氧血症（血氧饱和度下降≥5%至<90%）。运动或低氧血症时QTc离散度均无显著变化。比较有和没有血氧饱和度下降的患者，以及有和没有高基线QTc离散度值（60毫秒）的患者时，QTc离散度也没有显著变化。无运动时诱导的低氧血症也未能使QTc离散度恶化。
没有证据表明运动，即使与低氧血症相关，也会导致COPD患者出现心肌复极异常。
