Cabanes L, Lockhart A
Service des maladies cardio-vasculaires et service d'exploration fonctionnelle, hôpital Cochin, Paris.
Arch Mal Coeur Vaiss. 1990 Apr;83(4):549-53.
Effort dyspnea in cardiac failure corresponds to a subjective perception of difficulty in breathing which is itself secondary to a disproportion between the central bulbar respiratory regulation and the level of pulmonary ventilation attained. In cardiac failure, this situation is the result of dysfunction of both the respiratory apparatus and the skeletal striated muscle during exercise. During exercise a rise in left ventricular end diastolic pressure causes: a reduction in pulmonary compliance. The bronchial and alveolar capillaries drain into the pulmonary veins. The congestion of these capillaries and the resulting oedema makes the lung "stiffer"; an increase in the resistances of the small airways due to direct compression by congested bronchial vessels. The physiological dead space increases: the respiratory muscles ventilate pulmonary zones which are not perfused to no benefit. The reduction of pulmonary compliance, the increased resistances of the airways and of the physiological dead space all contribute to increase the work of the respiratory muscles. In addition to these mechanical phenomena, there is greater stimulation of the respiratory centre in the brain stem by the metabolic abnormalities of the skeletal striated muscles. During effort, they rapidly function under anaerobic conditions and the resulting hyperproduction of lactate and carbon dioxide stimulates the respiratory centres.
心力衰竭时的劳力性呼吸困难对应于一种主观的呼吸困难感觉，这种感觉本身继发于延髓中枢呼吸调节与所达到的肺通气水平之间的失衡。在心力衰竭中，这种情况是运动期间呼吸装置和骨骼肌功能障碍的结果。运动期间左心室舒张末期压力升高会导致：肺顺应性降低。支气管和肺泡毛细血管汇入肺静脉。这些毛细血管的充血及由此产生的水肿使肺“变硬”；由于充血的支气管血管直接压迫导致小气道阻力增加。生理死腔增加：呼吸肌对未灌注的肺区域进行通气而无益处。肺顺应性降低、气道阻力增加和生理死腔增加都有助于增加呼吸肌的工作量。除了这些机械现象外，骨骼肌的代谢异常对脑干呼吸中枢有更大的刺激作用。运动期间，它们在无氧条件下迅速发挥作用，由此产生的乳酸和二氧化碳过度生成刺激呼吸中枢。
