The aim of this study was to test the hypothesis that lung oedema caus
es an obstructive airway impairment, due to an increase in cholingeric
bronchial tone in patients with chronic heart failure (CHF). Ten pati
ents with CHF were tested by inhalation of ipratropium bromide and pla
cebo, given in sequential randomized order, in double-blind fashion, a
fter assessment of baseline lung function, both during acute cardiac d
ecompensation and after 8-10 days of adequate treatment. The decrease
in lung oedema was associated with a significant increase in vital cap
acity (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 bronchodilatat
ion during acute decompensation when FEV1 increased from 59+/-3.6 to 7
0+/-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 i
ncrease in FEV1 induced by ipratropium bromide was 286+/-32 ml at admi
ssion and only 111+/-15 ml after In conclusion, in chronic heart failu
re, airway obstruction is partially reversible after inhalation of an
anti-muscarmic drug, when lung oedema is present, supporting the hypot
hesis that lung oedema increases cholinergic bronchial tone.