Gas exchange responses to continuous incremental cycle ergometry exercise in primary pulmonary hypertension in humans

In patients suffering from primary pulmonary hypertension (PPH), a raised p ulmonary vascular resistance may limit the ability to increase pulmonary bl ood flow as work rate increases. We hypothesised that oxygen uptake ((V)ove r dot O-2) may not rise appropriately with increasing work rate during incr emental cardiopulmonary exercise tests. Nine PPH patients and nine normal s ubjects performed symptom-limited maximal continuous incremental cycle ergo metry exercise. Mean peak (V)over dot O-2 [1.00 (SD 0.22) compared to 2.58 (SD 0.64) l.min(-1)] and mean (V)over dot O-2 at lactic acidosis threshold [LAT, 0.73 (SD 0.17)compared to 1.46 (SD 0.21.l) ml.min(-1)] were much lowe r in patients than in normal subjects (both P < 0.01, two-way ANOVA with Tu key test). The mean rate of change of (V) over dot O-2 with increasing work rate above the LAT [5.9 (SD 2.1) compared to 9.4 (SD 1.3) ml.min(-1) W-1 P < 0.01)] was also much lower in patients than in normal subjects [apparent delta efficiency 60.3 (SD 38.8)% in patients compared to 31.0 (SD 4.9)% in normal subjects]. The patients displayed lower mean values of end-tidal pa rtial pressure of carbon dioxide than the normal subjects at peak exercise [29.7 (SD 6.8) compared to 43.4 (SD 5.8) mmHg, P < 0.01] and mean oxyhaemog lobin saturation [89.1 (SD 4.1) compared to 93.6 (SD 1.8)%, P < 0.05]. Mean ventilatory equivalents for CO2 [49.3 (SD 11.4) compared to 35.0 (SD 7.3), P < 0.05] and O-2 [44.2 (SD 10.7) compared to 29.9 (SD 5.1), P < 0.05] wer e greater in patients than normal subjects. The sub-normal slopes for the ( V)over dot O-2-work-rate relationship above the LAT indicated severe impair ment of the circulatory response to exercise in patients with PPH. The vent ilatory abnormalities in PPH suggested that the lung had become an ineffici ent gas exchange organ because of impaired perfusion of the ventilated lung .