Can Oxygen Transport Analysis Tell Us Why People With Heart Failure With Preserved Ejection Fraction Feel So Poorly?
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Article, see p 148
Heart failure (HF) with preserved ejection fraction (HFpEF) is a huge public health problem.1 There is no proven effective treatment. Patients with HFpEF are not able to engage in physical activity without developing symptoms of dyspnea and fatigue. This diminishes quality of life and is associated with increased mortality.1,2
To perform physical activity, we increase O2 consumption (Vo2). Oxygen transport is accomplished through convective and diffusive processes. Convective transport involves 2 steps: introduction of O2 into the lungs (alveolar ventilation) and transport from the lungs to the periphery in the circulation (cardiac output [CO]). Diffusive O2 transport describes 2 additional steps: movement of O2 across the alveolar-pulmonary capillary interface in the lung and unloading of O2 from hemoglobin in skeletal muscle capillaries (DM), where mitochondria consume it to make ATP. Impairments in any or several of these steps can constrain the ability of the body to increase Vo2 and thus perform activity.
When patients with HF display low peak Vo2, it is often assumed that this reflects a deficit in CO. However, according to the Fick principle, Vo2 is equal to the product of CO and the arterial-venous O2 content difference (AVO2diff). More than 20 years ago, Wilson and colleagues3 made the remarkable observation that 1/4 of patients with severe HF and reduced ejection fraction (HFrEF) actually display normal leg blood flow during exercise. Despite adequate convective O2 delivery, these patients developed profound leg fatigue and an accelerated increase in venous lactate, indicating a switch to anaerobic glycolysis. The patients were less able to increase AVO2diff during exercise, and this drove their low peak Vo2 rather than poor …