Abstract
Background Chronic heart failure (CHF) patients complain of breathlessness and fatigue. Respiratory muscle function is impaired in CHF patients and may contribute to their symptoms. β-blockers cause fatigue but have become part of the standard management of CHF. We explored the relation between respiratory muscle power in CHF and the effects of long-term β-blockade. Methods and Results A total of 52 CHF patients and 25 control subjects underwent echocardiography, peak exercise testing with metabolic gas exchange analysis, and measurement of forced vital capacity (FVC), forced expiratory volume in 1 second (FEV 1), peak inspiratory flow (PIF), and forced inspiratory volume in 1 second (FIV 1). Of the patients, 35 started β-blocker therapy and were tested again at 1 year. Patients had lower peak oxygen consumption (pV o 2) (19.3 [4.5] versus 37.3 [8.4] mL/kg/min, P < .0001), exercise time (414 [134] versus 817 [193] seconds, P < .0001), and anaerobic threshold (13.8 [3.8] versus 27.2 [8.2] mL/kg/min, P < .0001). Patients also had a steeper relationship between ventilation (V e) and carbon dioxide (CO 2) (V e/V co 2) (40.0 [6.8] versus 26.4 [2.0], P < .0001); lower FEV 1, FVC, and FIV 1 (89 [15] versus 111 [24]% expected, P < .0001, 80 [20] versus 94 [21]% expected, P < .001 and 2.5 [1.6] versus 3.0 (0.9) L, P < .02); and there was a correlation between pVo 2 and FIV 1 ( r = 0.24, P < .05) for the patients. The slope relating symptoms of breathlessness (Borg score) to ventilation (Borg/V e slope) also correlated with FIV 1 ( r = 0.36, P < .02). β-blocker therapy improved echocardiographic variables, but not pV o 2. There was no change in PIF or FIV 1. There was a significant reduction in FEV 1 after β-blocker treatment ( P < .01). Conclusion Inspiratory flows are impaired in patients with chronic heart failure and correlate with the degree of functional impairment. This may be due to a combination of respiratory muscle weakness and reduced lung compliance. The reduction in inspiratory capacity is not influenced by long-term β-blockade.
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