Respiratory gas analysis during exercise as a noninvasive measure of lactate concentration in chronic congestive heart failure.

Measurement of blood lactate during exercise in patients with chronic congestive heart failure provides a useful index of oxygen (O2) availability in working muscle. Bicarbonate buffering of lactate produces carbon dioxide (CO2) in excess of that resulting from oxidative metabolism. Therefore, calculation of excess CO2 production from measured CO2 production and O2 uptake may offer a noninvasive quantitative index of changes in blood lactate during exercise in these patients. To investigate this possibility, 22 patients with congestive heart failure and depressed left ventricular function were studied during progressive maximal upright bicycle exercise. Oxygen uptake, expired carbon dioxide, arterial lactate, O2 extraction, and cardiac output were measured at each 20 W incremental work load and peak exercise. Exercise increased VO2 from 3.5 +/- 0.9 ml/min/kg at rest to 13.1 +/- 2.9 ml/min/kg, O2 extraction from 49 +/- 9% at rest to 78 +/- 6%, lactate from 12 +/- 5 mg/dl at rest to 41 +/- 15 mg/dl, and cardiac index from 1.7 +/- 0.4 at rest to 3.8 +/- 1.2 liters/min/m2. The increase in lactate at each work load was linearly related to excess CO2 production (r = 0.92, p less than 0.01). Exercise was repeated the following day in 10 patients; measurements of excess CO2 production was highly reproducible (r = 0.98, p less than 0.01). Excess CO2 production also correlated with the decrease in bicarbonate produced by exercise (r = 0.81), supporting the hypothesis that excess CO2 is produced by bicarbonate buffering of lactate. Thus, calculation of excess carbon dioxide production from noninvasive measurement of respiratory gas exchange provides a reliable and reproducible method of continuously assessing alterations in lactate throughout bicycle exercise in patients with chronic congestive heart failure.