Beta-blockers and inspiratory pulmonary function in chronic heart failure

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 CHF. We explored the relation between respiratory muscle power in CHF and the effects of long-term beta-blockade.

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 < .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 (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 < .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 pV(O2) and FIV1 (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 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 FEV 1 after beta-blocker treatment (P < .01).

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 beta-blockade.