title: Beta-blockers and inspiratory pulmonary function in chronic heart failure.
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. 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.
  
  
  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 < .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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Academic Cardiology, Castle Hill Hospital, Cottingham, Hull, England.
authors.forename: Klaus K A
authors.initials: KK
authors.lastname: Witte
authors.forename: Andrew L
authors.initials: AL
authors.lastname: Clark
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000368:Aged; D016022:Case-Control Studies; D004452:Echocardiography; D005080:Exercise Test; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology*; D006801:Humans; D007320:Inspiratory Capacity / Q000187:drug effects; D011659:Pulmonary Gas Exchange; D012129:Respiratory Function Tests; D012132:Respiratory Muscles / Q000187:drug effects* / Q000503:physiopathology*; D013147:Spirometry; D013997:Time Factors
chemical_list: D000319:Adrenergic beta-Antagonists