β-blockers and inspiratory pulmonary function in chronic heart failure

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. beta-blockers cause fatigue but have become part of the standard management of CHE We explored the relation between respiratory muscle power in CHF and the effects of long-term beta-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 (FEV1), peak inspiratory flow (PIF), and forced inspiratory volume in 1 second (FIV1). Of the patients, 35 started beta-blocker therapy and were tested again at 1 year. Patients had lower peak oxygen consumption (pV(O2)) (19.3 [4.5] versus 37.3 [8.4] mL/kg/min, P <.000 1), exercise time (414 [134] versus 817 1,1931 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 (CO2) (V-E/V-CO2) (40.0 [6.8] versus 26.4 [2.0], P <.0001); lower FEV1, FVC, and FIV1 (89 [15] versus 111 [24] % expected, P <.000 1, 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 pV(O2) and FIV1 (r = 0.24, P < .05) for the patients. The slope relating symptoms of breathlessness (Borg score) to ventilation (Bora/V-E slope) also correlated with FIV1 (r = 0.36, P < .02). beta-blocker therapy improved echocardiographic variables, but not pV(O2). There was no change in PIF or FIV1. There was a significant reduction in FEV1 after beta-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 P-blockade.