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慢性心力衰竭中的运动性通气过度:与肺硬度和呼气流量受限的关系。

Exercise hyperpnea in chronic heart failure: relationships to lung stiffness and expiratory flow limitation.

作者信息

Agostoni Piergiuseppe, Pellegrino Riccardo, Conca Cristina, Rodarte Joseph R, Brusasco Vito

机构信息

Centro Cardiologico Monzino, IRCCS, Istituto di Cardiologia dell' Università degli Studi di Milano, IRCCS, Centro di Studio per le Ricerche Cardiovascolari del CNR, 20138 Milan, Italy.

出版信息

J Appl Physiol (1985). 2002 Apr;92(4):1409-16. doi: 10.1152/japplphysiol.00724.2001.

Abstract

The changes in breathing pattern and lung mechanics in response to incremental exercise were compared in 14 subjects with chronic heart failure and 15 normal subjects. In chronic heart failure subjects, exercise hyperpnea was achieved by increasing breathing frequency more than tidal volume. The rate of increase in breathing frequency with carbon dioxide output was inversely correlated (r = -0.61, P < 0.05) with dynamic lung compliance measured at rest, but not with static lung compliance either at rest or at maximum exercise. Although decrease in expiratory flow reserve near functional residual capacity in chronic heart failure occurred earlier with exercise than in the normal subjects (P < 0.01), it was not correlated with changes in breathing pattern or occurrence of tachypnea. Tachypnea was achieved in chronic heart failure subjects with an increase in duty cycle because of a greater than normal decrease in expiratory time with exercise. We conclude that in chronic heart failure preexisting increase in lung stiffness plays a significant role in causing tachypnea during exercise. The results of the present study do not support the hypothesis that dynamic compression of the airways downstream from the flow-limiting segment occurring during exercise contributes to hyperpnea.

摘要

对14名慢性心力衰竭患者和15名正常受试者在递增运动时的呼吸模式和肺力学变化进行了比较。在慢性心力衰竭患者中,运动性通气过度是通过增加呼吸频率而非潮气量实现的。呼吸频率随二氧化碳排出量的增加率与静息时测量的动态肺顺应性呈负相关(r = -0.61,P < 0.05),但与静息或最大运动时的静态肺顺应性均无相关性。尽管慢性心力衰竭患者在功能残气量附近呼气流量储备的降低在运动时比正常受试者出现得更早(P < 0.01),但它与呼吸模式的变化或呼吸急促的发生无关。慢性心力衰竭患者由于运动时呼气时间的下降幅度大于正常,通过增加呼吸比实现了呼吸急促。我们得出结论,在慢性心力衰竭中,预先存在的肺硬度增加在运动时导致呼吸急促中起重要作用。本研究结果不支持运动时在流量限制段下游气道的动态压缩导致通气过度的假说。

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