Heart failure increases the resistance to gas transfer across the alveolar-capillary interface. In different experimental conditions of vascular capillary injury, peculiar anatomical and functional abnormalities of the alveolar unit have been reported and consist of a disruption of its anatomical configuration and of a loss of fluid-flux regulation and gas exchange efficiency (i.e. "stress failure" of the alveolar-capillary membrane). In heart failure, the pathophysiological relevance of these changes has been only recently appreciated. Alveolar-capillary membrane conductance and capillary blood volume are subcomponents of lung diffusion capacity. A reduction of the former with an increase of the latter and consequent impairment of gas exchange are typical of heart failure syndrome. Alveolar-capillary membrane conductance abnormalities have been shown to be a sensitive index of the underlying lung tissue damage, bring an independent prognostic information and play a significant role in the pathogenesis of exercise limitation and ventilatory abnormalities. This review examines the current knowledge on this topic.