Worsening cardiac function in noncyanotic heart disease leads to a progressive decline in hemoglobin-oxygen affinity, acting as an adaptive mechanism to limited oxygen supply.
Reduced hemoglobin-oxygen affinity accompanies worsening cardiac function; leaves open whether modulating affinity improves outcomes in heart failure.
The relation between degree of cardiac functional impairment and changes in hemoglobin-oxygen affinity and 2,3-diphosphoglycerate (2,3-DPG) has been studied in 39 patients with noncyanotic heart disease. A progressive decline in hemoglobin-oxygen affinity was found with worsening cardiac function as assessed by cardiac index, arteriovenous oxygen (A-V O(2)) difference, and cardiac symptoms; this alteration in hemoglobin-oxygen binding represents a significant mechanism for adaptation to the limited oxygen supply imposed by the cardiac lesion. The highly significant correlation of mixed venous blood oxygen saturation (S[unk]V(VO2)) with 2,3-DPG and the position of the oxygen dissociation curve suggests that the level of deoxygenated hemoglobin is an important in vivo regulator of hemoglobin-oxygen affinity.
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Woodson et al. (1970) studied this question.
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