Abstract
Exercise intolerance is a hallmark of symptoms in patients with heart failure. In addition to reduced cardiac output, a series of impairments in pulmonary and vascular systems leads to decreases in oxygen delivery and availability in locomotor muscles. This contributes to exercise intolerance in heart failure. The oxy-hemoglobin dissociation curve is essentially a graph illustrating the relationship between the partial pressure of oxygen (PO2, X-axis) and oxygen saturation (SaO2, Y-axis) of hemoglobin. The rightward shift of the curve indicates that hemoglobin’s affinity for oxygen decreases and in turn, it may allow the release of more oxygen to tissues. In the present study, we discuss the pathophysiological impairment, which causes exercise intolerance in heart failure patients and suggest a strategy to improve exercise capacity without altering cardiac output via modulating the oxy-hemoglobin dissociation curve.
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