Ventilation during exercise in chronic heart failure
Ventilation during exercise in chronic heart failure
复制标题
慢性心力衰竭运动期间的通气
DOI：
10.1007/bf00810518
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发表时间：
1996
影响因子：
9.5
通讯作者：
M. Riley
中科院分区：
文献类型：
--
作者：
K. Wasserman;Y. ;M. Riley
摘要对于给定的工作或代谢率，慢性心力衰竭 (CHF) 患者对运动的通气反应高于正常人。
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氧气）。决定运动通气反应的因素有： 1) 二氧化碳的产生（
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CO2) 动脉 CO2 设定点（静息时的动脉 PCO2 (PaCO2)），3) 生理死腔/潮气量比 (Vd/Vt)，以及 4) 运动期间 PaCO2 的变化。本报告阐述了这些因素如何影响 CHF 患者对运动的通气反应。 对 31 名 CHF 患者（纽约心脏协会，2 级和 3 级）进行了研究，其中 18 名来自 Harbour-UCLA 医疗中心（自行车测力计锻炼），13 名来自贝尔法斯特女王大学（跑步机锻炼）。一组大小、年龄和性别相匹配的健康受试者作为对照受试者。分钟通气量（
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E) 与对照组人群相比，在 25 周和 60 周周期的 6 分钟以及低水平（2.5 km h−1 和 5% 等级）跑步机运动中，CHF 组的效果分别高出 48%、88% 和 43%。
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CHF 患者的 O2 动力学比对照组慢，其减慢与乳酸的增加成正比。然而，增加
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对于 CHF 和对照受试者，运动 6 分钟时高于休息时的 O2 大致相同。
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与对照组相比，25 瓦和 60 瓦循环的 CHF 患者 6 分钟时的氧气含量分别增加了 7% 和 34%，跑步机运动时的氧气含量分别增加了 19%。由于本研究中未测量 PaCO2，因此无法单独计算 CO2 设定点和 Vd/Vt。由于当 PaCO2 降低或 Vd/Vt 增加时，呼气末 PCO2 也会降低，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 增加的综合效应。由于在 60 周周期运动结束时，患者群体中的 PetCO2 显着降低（32 毫米汞柱与 41 毫米汞柱），因此 Vd/Vt 增加和/或 PaCO2 减少。由于 CHF 患者的静息 PaCO2 通常正常，因此 CHF 患者对运动的通气反应的增加可以最好地通过三种生理机制来解释：1）
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由于碳酸氢盐缓冲乳酸，继发于碳酸氢盐释放的二氧化碳，2) 继发于乳酸性酸中毒引起的过度通气的 PaCO2 减少，以及 3) 浪费的呼吸比例（死腔）增加。从数学上讲，这些因素相互作用，因此每个因素相对较小的变化都会导致
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E.
AbstractThe ventilatory response to exercise in patients with chronic heart failure (CHF) is greater than normal for a given work or metabolic rate (
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O2). The factors that determine the ventilatory response to exercise are: 1) the CO2 production (
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CO2) 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 (
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E) 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.
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O2 kinetics were slower in CHF patients than the control group, the slowing being proportional to the lactate increase. However, the increase in
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O2 above rest at 6 min of exercise was approximately the same for CHF and control subjects.
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O2 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 theVd/Vt could be individually calculated. Because end-tidal PCO2 will decrease when PaCO2 decreases orVd/Vt increases, the combined effect of PaCO2 change and increase inVd/Vt could be assessed from the difference between the patient and the control group. SincePetCO2 was significantly reduced in the patient population at the end of 60w cycle exercise (32 versus 41 mm Hg), either theVd/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
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CO2 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
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E.