Jennings G L, Esler M D
Clinical Research Unit, Alfred Hospital, Melbourne, Australia.
Circulation. 1990 Jan;81(1 Suppl):II5-13.
Congestive heart failure occurs when myocardial dysfunction is advanced. Although clinical manifestations and diminished functional capacity can be traced back to the poor cardiac contractile state, there are major modifying influences from a complex series of compensatory responses. These particularly involve the heart, vessels, kidneys, sympathetic nervous system, the renin-angiotensin system, and other hormone systems. Functional capacity is, therefore, determined by the sum of the effects of the original cardiac insult and the effects, beneficial and adverse, of the secondary events. Functional capacity relates closely to prognosis only in the most severely disabled patients. The latter is mainly related to the extent of ventricular dysfunction, and there can be independent contributions from arrhythmias and sympathetic activity. Measures of resting parameters of cardiac contractility, hemodynamics, or neurohumoral responses are, therefore, of no value in predicting functional capacity but can be useful in examining outlook or examining mechanisms of disease and therapy. Exercise measurements are necessary because adequate resting performance can disguise major limitations in cardiac reserve. Measurement of functional capacity can be used to quantify the effects of therapy on daily living and to give an indication of the overall response of the body to major cardiac inadequacy. Limitation of exercise capacity, the earliest symptom of heart failure, can be quantified during a graded exercise test. Measurements of cardiac output and hemodynamic variables during exercise quantify the extent to which the cardiovascular system can increase performance to meet the demands of exercise. Work capacity and maximum oxygen capacity indicate the limits of physical performance, whereas determination of the anaerobic threshold indicates the highest level of exercise at which cardiorespiratory mechanisms are able to provide adequate oxygen supply to maintain aerobic metabolism in working skeletal muscle.
当心肌功能障碍进展到晚期时，会发生充血性心力衰竭。尽管临床表现和功能能力下降可追溯到心脏收缩功能不佳，但一系列复杂的代偿反应会产生重大的调节影响。这些影响尤其涉及心脏、血管、肾脏、交感神经系统、肾素 - 血管紧张素系统以及其他激素系统。因此，功能能力取决于原发性心脏损伤的影响以及继发性事件的有益和有害影响的总和。仅在最严重残疾的患者中，功能能力才与预后密切相关。后者主要与心室功能障碍的程度有关，心律失常和交感神经活动也可能有独立的影响。因此，心脏收缩力、血流动力学或神经体液反应的静息参数测量对预测功能能力没有价值，但可用于评估预后或研究疾病及治疗机制。运动测量是必要的，因为静息状态下的良好表现可能掩盖心脏储备的主要限制。功能能力的测量可用于量化治疗对日常生活的影响，并表明身体对严重心脏功能不全的总体反应。运动能力受限是心力衰竭的最早症状，可在分级运动试验中进行量化。运动期间的心输出量和血流动力学变量测量可量化心血管系统能够提高性能以满足运动需求的程度。工作能力和最大氧容量表明身体表现的极限，而无氧阈值的测定则表明心肺机制能够提供足够氧气供应以维持工作骨骼肌有氧代谢的最高运动水平。
