It is proposed that lung function may be altered in heart failure either through (A) vascular engorgement in the mucosal plexus of the bronchial circulation, or through (B) expansion of the pulmonary circulation, interstitial pulmonary edema , and/or other sources competing for intrathoracic space displacing airspace by compressing the entire airway structure, including the bronchiole wall. In the latter example, wall thickness remains relatively unchanged. Also possible, but not shown, is the potential impact of smooth muscle proliferation.