OXYGEN-UPTAKE KINETICS IN RESPONSE TO EXERCISE IN PATIENTS WITH PULMONARY VASCULAR-DISEASE

The increase in muscular oxygen consumption that accompanies the onset of exercise is accomplished by increases in blood flow and arterial-venous O2 difference. These processes are reflected in a similar increase in pulmonary oxygen uptake (VO2), which rises in a dynamic pattern having two components and with an overall time course that may be characterized as an exponential. Because the immediate determinants of VO2 are the blood flow and respiratory gas composition in the pulmonary circulation, it was hypothesized that VO2 kinetics at exercise onset would be abnormal in patients with pulmonary vascular disease. To test this, 10 patients with pulmonary hypertension and two with pulmonary hypoperfusion caused by congenital heart disease performed constant work rate (15 +/- 16 SD watt) exercise on an upright cycle ergometer, with breath-by-breath measurement of respiratory gas exchange for determination of VO2 kinetics. The phase 1 increase in VO2, comprising approximately the first 30 s of exercise, was small (18 +/- 15 SD % above resting VO2). The time constant for the phase 11 increase in VO2 averaged 74 +/- 16 s, and the mean response time for attainment of the exercise steady state (75 +/- 17 SD s) was prolonged compared with normal values for the same work rate exercise (approximately 100 to 130% increase in phase 1, and mean response time < 25 s). In two patients who underwent surgical procedures substantially improving pulmonary hemodynamics, VO2 kinetics also improved. These findings are consistent with the concept that VO2 kinetics may be limited by pulmonary hemodynamics in the presence of disease. Because the measurements are noninvasive and well tolerated, analysis of gas exchange kinetics may be useful in the evaluation of patients with pulmonary vascular disorders.