Circulation, Vol 84, 605-612, Copyright © 1991 by American Heart Association
R Hachamovitch, HV Brown and SA Rubin
BACKGROUND. The output of carbon dioxide (VCO2) is controlled by both
hemodynamics and ventilation. To understand VCO2 in patients who have
chronic heart failure (CHF), we studied 14 patients who had New York Heart
Association functional class III failure by measurements of hemodynamics,
ventilation, and arterial and venous blood gases at rest and at 50 W of
cycle ergometry exercise. METHODS AND RESULTS. Fick principle analysis of
VCO2 showed that because of a limited increase in cardiac output, CHF
patients widened their venoarterial CO2 content difference from 4.9 +/- 3.5
ml/dl at rest to 11.1 +/- 4.0 ml/dl with exercise (p less than 0.05). This
increase in CO2 content difference was achieved with no change in venous
CO2 content (from 54.3 +/- 3.3 ml/dl at rest to 54.5 +/- 4.8 ml/dl at
exercise, p = NS); however, there was a decrease of arterial CO2 content
(from 49.4 +/- 3.7 ml/dl at rest to 43.4 +/- 2.3 ml/dl with exercise, p
less than 0.05). Modeling of the CO2 tension-content relation showed that
there would have been a small, nonproportional increase of venous CO2
content as venous CO2 tension increased from 43.2 +/- 1.8 mm Hg at rest to
55.3 +/- 4.2 mm Hg during exercise (p less than 0.05); however, the
development of metabolic acidosis during exercise entirely blunted the
increase of CO2 content. In contrast, both the shape of the tension-content
relation and the acidosis of exercise further influenced the decrease of
arterial CO2 content as arterial CO2 tension decreased from 37.0 +/- 2.9 mm
Hg at rest to 32.0 +/- 3.4 mm Hg during exercise (p less than 0.05) as a
result of excess ventilation. CONCLUSIONS. In CHF patients during exercise,
the circulatory limitations imposed by a low cardiac output on VCO2 are
compensated by a widened venoarterial CO2 content difference. The content
difference is not widened through an increase of venous CO2 content but
rather by a decrease of arterial CO2 content caused by arterial hypocapnia
and metabolic acidosis.
ARTICLES
Respiratory and circulatory analysis of CO2 output during exercise in chronic heart failure
Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
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