Wilson J R, Mancini D M
Department of Medicine, University of Pennsylvania, Philadelphia 19104.
J Am Coll Cardiol. 1993 Oct;22(4 Suppl A):93A-98A. doi: 10.1016/0735-1097(93)90469-h.
Exertional intolerance is a major clinical problem in ambulatory patients with chronic heart failure and is associated with both muscle fatigue and dyspnea. The increased muscle fatigability is most likely caused by a combination of muscle underperfusion and muscle deconditioning; patients frequently exhibit skeletal muscle atrophy, altered muscle metabolism and reduced mitochondrial-based enzyme levels, consistent with deconditioning. The muscle underperfusion is largely due to impaired arteriolar vasodilation within exercising muscle. Exertional dyspnea appears to be due to increased respiratory muscle work mediated by excessive ventilation and decreased lung compliance. Both excessive carbon dioxide production, secondary to increased muscle lactate release, and increased lung dead space contribute to the excessive ventilation. Decreased lung compliance is caused by chronic pulmonary congestion and fibrosis. Optimal management of exercise intolerance in patients with heart failure requires an understanding of the role of these multiple potential contributors to exertional fatigue and dyspnea.
运动耐力下降是慢性心力衰竭门诊患者的一个主要临床问题，与肌肉疲劳和呼吸困难均有关联。肌肉易疲劳性增加很可能是由肌肉灌注不足和肌肉失健联合所致；患者常表现出骨骼肌萎缩、肌肉代谢改变以及基于线粒体的酶水平降低，这与失健相符。肌肉灌注不足很大程度上归因于运动肌肉内小动脉血管舒张受损。运动性呼吸困难似乎是由于过度通气介导的呼吸肌工作增加以及肺顺应性降低所致。继发于肌肉乳酸释放增加的二氧化碳产生过多以及肺死腔增加均导致过度通气。肺顺应性降低是由慢性肺充血和纤维化引起的。心力衰竭患者运动不耐受的最佳管理需要了解这些导致运动性疲劳和呼吸困难的多种潜在因素所起的作用。
