Cardiopulmonary function in patients with pulmonary hypertension.

The effects ofpulmonary hypertension on cardiopulmonary function were investigated by ventilatory, haemodynamic, and metabolic studies at rest and during exercise. The studies were carried out in 12 patients with primary, thromboembolic, or residual pulmonary hypertension after surgical closure of intracardiac defects, and in II patients with pulmonary hypertension secondary to obstructive lung disease. The findings have been compared with earlier published results of similar studies, performed in other situations associated with pulmonary hypertension. The cardiac output is reduced in mostforms ofpulmonary hypertension. A relation was found between the reduction in exercise output and the level of pulmonary arterial pressure. Exceptions occur, indicating the contribution of additionalfactors to the circulatory response. Lungfunction tests usually gave normal results in primary thromboembolic and residual pulmonary hypertension. The variability offindings in the different conditions associated with pulmonary hypertension suggests that increasedpulmonary arterial pressure, per se, has no effect on lungfunction. Some degree of exercise hyperventilation is present in mostforms ofpulmonary hypertension. This is usually pronounced in primary and thromboembolic pulmonary hypertension but it is less pronounced in obstructive lung disease. The factors determining exercise ventilation in the various forms ofpulmonary hypertension are discussed. Evidence is given that tissue hypoxia may be implicated in the genesis of the mild hyperventilation seen in lung disease. In primary and thromboembolic pulmonary hypertension the haemodynamic abnormalities, changes in arterial blood composition, or tissue hypoxia are apparently not responsible for the excessive ventilatory response. It is believed that hyperventilation in these conditions is a consequence of abnormal receptor impulses from the lungs.