title: Respiratory and circulatory analysis of CO2 output during exercise in chronic heart failure.
abstract: 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.
  
  
  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.
authors.affiliation: Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
authors.forename: R
authors.initials: R
authors.lastname: Hachamovitch
authors.forename: H V
authors.initials: HV
authors.lastname: Brown
authors.forename: S A
authors.initials: SA
authors.lastname: Rubin
mesh_terms: D001692:Biological Transport; D002245:Carbon Dioxide / Q000097:blood; D002303:Cardiac Output, Low / Q000097:blood / Q000503:physiopathology*; D002908:Chronic Disease; D015444:Exercise; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008954:Models, Biological; D012119:Respiration
chemical_list: D002245:Carbon Dioxide