Chronic heart failure (CHF) disturbs the alveolar–capillary interface and increases the resistance to gas transfer. Alveolar–capillary membrane conductance (DM) and capillary blood volume (Vc) are subcomponents of the lung diffusion capacity. Elevation of the capillary pressure causes alveolar–capillary membrane stress failure (i.e. increase in capillary permeability to water and ions, and disruption of local regulatory mechanisms for gas exchange), leading to a decrease in DM, an increase in Vc and subsequent impairment of diffusion capacity. Renewed recent interest in abnormalities in lung diffusion in patients with CHF has brought about new pathophysiological insights. A significant contribution of the altered gas transfer to the pathogenesis of exercise limitation and ventilatory abnormalities has been reported, and DM has been identified as the best lung function predictor of oxygen uptake at peak exercise. This review examines the pathophysiological and clinical significance of assessing lung diffusion capacity in patients with CHF.

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