Wasserman K, Zhang Y Y, Riley M S
Queens University Belfast, North Ireland.
Basic Res Cardiol. 1996;91 Suppl 1:1-11. doi: 10.1007/BF00810518.
The ventilatory response to exercise in patients with chronic heart failure (CHF) is greater than normal for a given work or metabolic rate (VO2). The factors that determine the ventilatory response to exercise are: 1) the CO2 production (VCO2), 2) the arterial CO2 set-point (arterial PCO2 (PaCO2) at rest), 3) the physiological dead space/tidal volume ratio (VD/VT), and 4) the change in PaCO2 during exercise. This report illustrates how each of these factors might influence the ventilatory response to exercise in CHF patients. Thirty-one CHF patients (New York Heart Association, Classes 2 and 3) were studied, 18 from Harbor-UCLA Medical Center (cycle-ergometer exercise) and 13 from Queen's University at Belfast (treadmill exercise). A group of healthy subjects matched for size, age and gender served as control subjects. Minute ventilation (VE) was 48, 88 and 43% greater in the CHF groups compared to the control population at 6 min of the 25w and 60w cycle and low level (2.5 km h-1 and 5% grade) treadmill exercise, respectively. VO2 kinetics were slower in CHF patients than the control group, the slowing being proportional to the lactate increase. However, the increase in VO2 above rest at 6 min of exercise was approximately the same for CHF and control subjects. VCO2 at 6 min increased in the CHF patients by 7% and 34% for 25 and 60 watts cycle and 19% for treadmill exercise, respectively, compared to the control group. Because PaCO2 was not measured in this study, neither CO2 set-point nor the VD/VT could be individually calculated. Because end-tidal PCO2 will decrease when PaCO2 decreases or VD/VT increases, the combined effect of PaCO2 change and increase in VD/VT could be assessed from the difference between the patient and the control group. Since PETCO2 was significantly reduced in the patient population at the end of 60w cycle exercise (32 versus 41 mm Hg), either the VD/VT was increased and/or the PaCO2 was reduced. Because the resting PaCO2 is generally normal in CHF patients, the increase in the ventilatory response to exercise in patients with CHF can best be accounted for by three physiological mechanisms: 1) an increase in VCO2 secondary to CO2 release from bicarbonate as it buffers lactic acid, 2) the reduction in PaCO2 secondary to the lactic acidosis-induced hyperventilation, and 3) an increase in the fraction of breath that is wasted (dead space). Mathematically, these factors interact so that relatively small changes in each cause large changes in VE.
对于慢性心力衰竭（CHF）患者，在给定的工作量或代谢率（VO₂）下，其运动时的通气反应高于正常水平。决定运动通气反应的因素有：1）二氧化碳产生量（VCO₂），2）动脉二氧化碳设定点（静息时的动脉血二氧化碳分压（PaCO₂）），3）生理死腔/潮气量比值（VD/VT），以及4）运动期间PaCO₂的变化。本报告阐述了这些因素中的每一个如何可能影响CHF患者的运动通气反应。研究了31例CHF患者（纽约心脏协会心功能分级为2级和3级），其中18例来自哈伯-加州大学洛杉矶分校医学中心（采用自行车测力计进行运动），13例来自贝尔法斯特女王大学（采用跑步机进行运动）。一组在体型、年龄和性别上匹配的健康受试者作为对照。在25瓦和60瓦自行车运动以及低强度（2.5千米/小时和5%坡度）跑步机运动6分钟时，CHF组的分钟通气量（VE）分别比对照组高48%、88%和43%。CHF患者的VO₂动力学比对照组慢，其减慢程度与乳酸增加成正比。然而，运动6分钟时CHF患者高于静息时的VO₂增加量与对照组大致相同。与对照组相比，CHF患者在25瓦和60瓦自行车运动6分钟时的VCO₂分别增加了7%和34%，在跑步机运动时增加了19%。由于本研究未测量PaCO₂，因此无法单独计算二氧化碳设定点或VD/VT。由于当PaCO₂降低或VD/VT增加时，呼气末二氧化碳分压会降低，因此可以根据患者与对照组之间的差异来评估PaCO₂变化和VD/VT增加的综合影响。由于在60瓦自行车运动结束时患者组的呼气末二氧化碳分压（PETCO₂）显著降低（32对41毫米汞柱），因此要么VD/VT增加，要么PaCO₂降低。由于CHF患者静息时的PaCO₂通常正常，CHF患者运动通气反应增加最好由三种生理机制来解释：1）由于碳酸氢盐缓冲乳酸时释放二氧化碳导致VCO₂增加，2）乳酸酸中毒引起的过度通气导致PaCO₂降低，以及3）无效呼吸（死腔）部分增加。从数学角度来看，这些因素相互作用，以至于每个因素相对较小的变化都会导致VE发生较大变化。
