Abstract
Hypoxia is common in many chronic lung diseases. Beyond pulmonary considerations, delivery of oxygen (O(2)) to the tissues and subsequent O(2) utilisation is also determined by other factors including red blood cell mass and iron status; consequently, disruption to these mechanisms provides further physiological strains on an already stressed system. O(2) availability influences ventilation, regulates pulmonary blood flow and impacts gene expression throughout the body. Deleterious effects of poor tissue oxygenation include decreased exercise tolerance, increased cardiac strain and pulmonary hypertension in addition to pathophysiological involvement of multiple other organs resulting in progressive frailty. Increasing inspired O(2) is expensive, disliked by patients and does not normalise tissue oxygenation; thus, other strategies that improve O(2) delivery and utilisation may provide novel therapeutic opportunities in patients with lung disease. In this review, we focus on the rationale and possibilities for doing this by increasing haemoglobin availability or improving iron regulation.