Bronchodilating effect of ipratropium bromide in heart failure

Abstract

The aim of this study was to test the hypothesis that lung oedema causes an obstructive airway impairment, due to an increase in cholinergic bronchial tone in patients with chronic heart failure (CHF). Ten patients with CHF were tested by inhalation of ipratropium bromide and placebo, given in sequential randomized order, in double-blind fashion, after assessment of baseline lung function, both during acute cardiac decompensation and after 8-10 days of adequate treatment. The decrease in lung oedema was associated with a significant increase in vital capacity (VC) (from 70 ± 4.4 to 83 ± 5.4% pred), forced expiratory volume in one second (FEV1) (from 59 ± 3.6 to 72 ± 4.6% pred), FEV1/VC (from 61 ± 2.8 to 64 ± 2.3%) and residual volume (RV) (from 94 ± 7.9 to 99 ± 6.8% pred). Ipratropium bromide produced a far better bronchodilatation during acute decompensation when FEV1 increased from 59 ± 3.6 to 70 ± 3.7% pred, than after intensive treatment for heart failure, when FEV1 increased from 72 ± 4.6 to 76 ± 4.8% pred. The maximum absolute increase in FEV1 induced by ipratropium bromide was 286 ± 32 ml at admission and only 111 ± 15 ml after treatment. In conclusion, in chronic heart failure, airway obstruction is partially reversible after inhalation of an anti-muscarinic drug, when lung oedema is present, supporting the hypothesis that lung oedema increases cholinergic bronchial tone.