Matsumoto A, Itoh H, Eto Y, Kobayashi T, Kato M, Omata M, Watanabe H, Kato K, Momomura S
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
J Am Coll Cardiol. 2000 Jul;36(1):242-9. doi: 10.1016/s0735-1097(00)00702-6.
We measured end-tidal CO2 pressure (PETCO2) during exercise and investigated the relationship between PETCO2 and exercise capacity, ventilatory parameters and cardiac output to determine the mechanism(s) of changes in this parameter.
It is unclear whether PETCO2 is abnormal at rest and during exercise in cardiac patients.
Cardiac patients (n = 112) and normal individuals (n = 29) performed exercise tests with breath-by-breath gas analysis, and measurement of cardiac output and arterial blood gases.
PETCO2 was lower in patients than in normal subjects at rest and decreased as the New York Heart Association class increased, whereas the partial pressure of arterial CO2 did not differ among groups. Although PETCO2 increased during exercise in patients, it remained lower than in normal subjects. PETCO2 in relation to cardiac output was similar in patients and normal subjects. PETCO2 at the respiratory compensation point was positively correlated with the O2 uptake (r = 0.583, p < 0.0001) and the cardiac index at peak exercise (r = 0.582, p < 0.0001), and was negatively correlated with the ratio of physiological dead space to the tidal volume. The sensitivity and specificity of PETCO2 to predict an inadequate cardiac output were 76.6% and 75%, respectively, when PETCO2 at respiratory compensation point and a cardiac index at peak exercise that were less than the respective control mean-2 SD values were considered to be abnormal.
PETCO2 was below normal in cardiac patients at rest and during exercise. PETCO2 was correlated with exercise capacity and cardiac output during exercise, and the sensitivity and specificity of PETCO2 regarding decreased cardiac output were good. PETCO2 may be a new ventilatory abnormality marker that reflects impaired cardiac output response to exercise in cardiac patients diagnosed with heart failure.
我们测量了运动期间的呼气末二氧化碳分压(PETCO2),并研究了PETCO2与运动能力、通气参数和心输出量之间的关系,以确定该参数变化的机制。
目前尚不清楚心脏病患者在静息和运动时PETCO2是否异常。
心脏病患者(n = 112)和正常个体(n = 29)进行了逐次呼吸气体分析的运动测试,并测量了心输出量和动脉血气。
静息时患者的PETCO2低于正常受试者,且随着纽约心脏协会分级增加而降低,而动脉二氧化碳分压在各组间无差异。虽然患者运动期间PETCO2升高,但仍低于正常受试者。患者和正常受试者中PETCO2与心输出量的关系相似。呼吸补偿点时的PETCO2与摄氧量(r = 0.583,p < 0.0001)和运动峰值时的心指数(r = 0.582,p < 0.0001)呈正相关,与生理死腔与潮气量之比呈负相关。当将呼吸补偿点时的PETCO2和运动峰值时的心指数小于各自对照平均值减2个标准差的值视为异常时,PETCO2预测心输出量不足的敏感性和特异性分别为76.6%和75%。
心脏病患者在静息和运动时PETCO2低于正常水平。PETCO2与运动能力和运动期间的心输出量相关,且PETCO2对于心输出量降低的敏感性和特异性良好。PETCO2可能是一种新的通气异常标志物,反映了诊断为心力衰竭的心脏病患者运动时心输出量反应受损。