ABSTRACT
Pulmonary hypertension (PH) is defined as mean resting pulmonary artery pressures greater than 25 mm Hg; PH may arise from a number of different disease processes. Idiopathic pulmonary artery hypertension (PH Type I) produces the most characteristic CPET abnormalities, but those exercise findings are also shared by the other PH diagnoses to a variable degree. The initial disease symptoms are loss of exercise tolerance associated with increased exertional dyspnea. CPET provides the most useful information when it is utilized early in the patient's disease course. (For patients with severe disease and exertional syncope, a maximal exercise test is contraindicated.) Both heart failure and PH patients demonstrate a decreased maximal oxygen uptake, but the PH patients demonstrate an exceptionally brisk ventilation response to exercise, with ventilatory equivalents for CO2 (VE/VCO2) well in excess of 35 liters/liter CO2. Coupled with this abnormality is a high maximal heart rate with the decreased maximal oxygen uptake, leading to a low maximal O2 pulse. In addition, the O2 pulse ordinarily fails to increase normally following the onset of exercise, suggesting progressive loss of forward stroke volume at higher heart rates. The most characteristic PH CPET abnormalities are revealed by exercise arterial blood gas measurements for gas exchange calculations. The physiologic dead space during exercise in PH patients remains abnormally high throughout exercise. Although arterial oxygen saturation measurements with PH hyperventilation may remain near-normal, the A-a O2 difference is progressively increased.
