Reindl I, Kleber F X
Klinik für Innere Medizin I, Klinikum Charité, Humboldt Universität zu Berlin.
Basic Res Cardiol. 1996;91 Suppl 1:37-43. doi: 10.1007/BF00810522.
Hyperpnea in chronic heart failure occurs even in the absence of considerable impairment of lung function. It is caused by altered respiratory pattern with rapid shallow breathing and ventilation-perfusion mismatch, so far thought to be irreversible.
To test the underlying pathophysiologic disorders and the reversibility of this hyperpnea, i.e., the increased ventilatory response to exercise and its impact on exercise tolerance, 17 patients with chronic heart failure were evaluated before and 4 weeks after adjustment of heart failure therapy with diuretics and ACE inhibitors, and results were compared with normal volunteers.
Ventilatory response to exercise was measured during treadmill exercise by calculation of the slope of the linear relation between minute ventilation (VE) and carbon dioxide output (VCO2) and compared to NYHA class, oxygen consumption at the gas exchange anaerobic threshold (VO2 AT), maximal oxygen uptake (VO2 max) and ventilation of physiological dead space.
VE vs VCO2 slope was related to severity of heart failure (NYHA class). Elevation of VE vs VCO2 slope was strongly correlated to elevated ventilation of physiologic dead space. Patients were divided into responders (significant decrease of VE vs VCO2 slope of at least 5 l/l I CO2) and nonresponders (decrease of VE vs VCO2 slope less than 5 I or increase). Responders revealed an increase of VO2 AT (7.4 +/- 2.6 to 11.7 +/- 2.1 ml O2/kg/min; p = 0.01) and VO2 max (11.2 +/- 2.8 to 17.4 +/- 5.3; p = 0.005), while nonresponders showed a non significant decrease of oxygen consumption (VO2 AT 9.6 +/- 3.7 to 9.0 +/- 3.7; peak VO2 14.6 +/- 6.1 to 14.4 +/- 6.4), despite adjusted heart failure therapy.
Exercise hyperpnea in heart failure is mainly caused by ventilation of excess physiologic dead space and strongly contributes to severity of symptoms. Ventilatory response to exercise can be improved by adjustment of heart failure therapy in a considerable proportion of patients. Improvement is associated with an increase in aerobic capacity. Ventilation-perfusion mismatch is a major and modifiable factor determining exercise tolerance in patients with chronic heart failure.
慢性心力衰竭患者即使在肺功能未受到严重损害时也会出现呼吸急促。其原因是呼吸模式改变，表现为快速浅呼吸以及通气-灌注不匹配，目前认为这种情况是不可逆的。
为了检测这种呼吸急促潜在的病理生理紊乱情况以及其可逆性，即运动时通气反应增加及其对运动耐力的影响，我们对17例慢性心力衰竭患者在使用利尿剂和血管紧张素转换酶抑制剂调整心力衰竭治疗前和治疗4周后进行了评估，并将结果与正常志愿者进行了比较。
在跑步机运动期间，通过计算分钟通气量（VE）与二氧化碳排出量（VCO2）之间线性关系的斜率来测量运动时的通气反应，并与纽约心脏协会（NYHA）心功能分级、气体交换无氧阈时的耗氧量（VO2 AT）、最大摄氧量（VO2 max）以及生理无效腔通气进行比较。
VE与VCO2斜率与心力衰竭的严重程度（NYHA分级）相关。VE与VCO2斜率升高与生理无效腔通气增加密切相关。患者被分为反应者（VE与VCO2斜率显著降低至少5升/升二氧化碳）和无反应者（VE与VCO2斜率降低小于5升或升高）。反应者的VO2 AT（从7.4±2.6升至11.7±2.1毫升氧气/千克/分钟；p = 0.01）和VO2 max（从11.2±2.8升至17.4±5.3；p = 0.005）有所增加，而无反应者尽管进行了心力衰竭治疗调整，耗氧量仍出现不显著下降（VO2 AT从9.6±3.7降至9.0±3.7；峰值VO2从14.6±6.1降至14.4±6.4）。
心力衰竭患者的运动性呼吸急促主要由过多的生理无效腔通气引起，并严重影响症状的严重程度。在相当一部分患者中，通过调整心力衰竭治疗可以改善运动时的通气反应。这种改善与有氧运动能力的增加相关。通气-灌注不匹配是决定慢性心力衰竭患者运动耐力的一个主要且可改变的因素。
