I Reindl1, F X Kleber. 1. Klinik für Innere Medizin I, Klinikum Charité, Humboldt Universität zu Berlin.
Abstract
BACKGROUND: 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. OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: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. OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
Authors: J Theodore; E D Robin; A J Morris; C M Burke; S W Jamieson; A Van Kessel; E B Stinson; N E Shumway Journal: Chest Date: 1986-01 Impact factor: 9.410
Authors: T Tomita; H Takaki; Y Hara; F Sakamaki; T Satoh; S Takagi; Y Yasumura; N Aihara; Y Goto; K Sunagawa Journal: Heart Date: 2003-04 Impact factor: 5.994
Authors: Lluis Albesa-Albiol; Noemí Serra-Payá; María Ana Garnacho-Castaño; Lluis Guirao Cano; Eulogio Pleguezuelos Cobo; José Luis Maté-Muñoz; Manuel V Garnacho-Castaño Journal: PLoS One Date: 2019-05-21 Impact factor: 3.240