Pathophysiology and treatment of alveolar-capillary dysfunction in chronic heart failure

Marco Guazzi

Heart failure increases the resistance to gas transfer across the alveolar–capillary membrane. Disruption of the alveolar anatomical configuration and impairment of cellular pathways involved in the fluid–flux regulation and gas-exchange efficiency (i.e., ‘stress failure’ of the alveolar–capillary membrane) has been well characterized in different experimental settings of vascular–capillary injury. In heart failure, the appreciation of the pathophysiologic relevance of alveolar stress failure continues to grow. Alveolar–capillary membrane conductance and capillary blood volume are the subcomponents of lung-diffusion capacity. An alveolar–capillary membrane conductance reduction with a trend of capillary blood volume to increase and with consequent impairment of gas exchange, are typical of the heart-failure syndrome. Alveolar–capillary membrane conductance abnormalities have been shown to reflect the underlying lung-tissue damage, to bring an independent prognostic information and to play a significant role in the pathogenesis of exercise limitation and ventilatory abnormalities. This review focuses on the current knowledge on this topic.