Pathophysiological adaptations to walking and cycling in primary pulmonary hypertension
In patients suffering from primary pulmonary hypertension (PPH), a raised pulmonary vascular resistance may limit the ability to increase pulmonary blood flow as work rate increases. We hypothesised that oxygen uptake (V˙O2) may not rise appropriately with increasing work rate during incremental cardiopulmonary exercise tests. Nine PPH patients and nine normal subjects performed symptom-limited maximal continuous incremental cycle ergometry exercise. Mean peak V˙O2 [1.00 (SD 0.22) compared to 2.58 (SD 0.64) l · min−1] and mean V˙O2 at lactic acidosis threshold [LAT, 0.73 (SD 0.17) compared to 1.46 (SD 0.21 · l) ml · min−1] were much lower in patients than in normal subjects (both P < 0.01, two-way ANOVA with Tukey test). The mean rate of change of V˙O2 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 δ 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 partial pressure of carbon dioxide than the normal subjects at peak exercise [29.7 (SD 6.8) compared to 42.4 (SD 5.8) mmHg, P < 0.01] and mean oxyhaemoglobin 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 O2 [44.2 (SD 10.7) compared to 29.9 (SD 5.1), P < 0.05] were greater in patients than normal subjects. The sub-normal slopes for the V˙O2-work-rate relationship above the LAT indicated severe impairment of the circulatory response to exercise in patients with PPH. The ventilatory abnormalities in PPH suggested that the lung had become an inefficient gas exchange organ because of impaired perfusion of the ventilated lung.