The decrease in VO2 requirement in heart failure patients during exercise is likely due to blood redistribution as a compensatory mechanism for exercise intolerance.
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May reflect compensatory blood redistribution in HF; hypothesis-generating and requires prospective validation.
To assess the compensatory change in oxygen uptake (VO2) kinetics during exercise in patients with heart failure, we performed cardiopulmonary exercise testing using a cycle ergometer in 29 cardiac patients and 18 normal subjects. The work rate increased linearly (1w/6sec) after a 4 min, 20w warm-up. The ratio of increase in VO2 to increase in work rate (delta VO2/delta WR) was determined by linear regression of VO2 plots. Cardiac output by dye dilution method and plasma norepinephrine concentration (NE) were measured at rest and 20w warm-up. VO2 at rest and at 20w warm-up and delta VO2/delta WR decreased significantly with increasing severity in NYHA functional classification. delta VO2/delta WR showed significant negative correlation to the difference in NE levels at rest and at 20w (r = -0.69, p less than 0.001). The delta values of arteriovenous O2 content difference, calculated using Fick's principle, and cardiac index from rest to 20w warm-up failed to show significant relationship to delta VO2/delta WR. These results suggest that the decrease in VO2 requirement in heart failure patients is due probably to blood redistribution during exercise as a compensatory mechanism for exercise intolerance.
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Itoh et al. (1992) studied this question.
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