Pulmonary functions may be considerably influenced by changes in pulmonary haemodynamics in congenital heart disease. In analysing this problem we have found resting hyperventilation to be a common finding in these patients. There are few published studies on this relation and those that exist do not agree. In the present study the resting hyperventilation has been related to the pulmonary circulatory changes in a group of adults with atrial septal defect with particular regard being paid to the question whether there exists any correlation between the resting ventilation and pulmonary hypertension or the magnitude of the left-to-right shunt.
SUBJECTS AND METHODSStudies have been made of 37 patients with atrial septal defect of the secondary type (26 women and 11 men), whose ages ranged from 15 to 65 years (average 29-8 years). All other congenital heart diseases have been excluded, with the exception of concomitant anomalous pulmonary venous drainage.The diagnosis was confirmed by clinical, x-ray, and electrocardiographic examination, and in all patients by cardiac catheterization. This was performed in the usual way without any premedication in the fasting state. The pressure in all compartments of the right heart as well as the vascular pulmonary resistance was measured. The patients were divided into two groups according to their pulmonary artery pressure; 20 mm. Hg of mean pulmonary arterial pressure was considered to be upper normal limit. In the first group with normal pulmonary pressure were 26 patients (average age 27 years); in the second group 11 patients with pulmonary hypertension ranging from 23 to 96 mm. Hg of mean pulmonary arterial pressure (average age 39 years). In only one patient (Case 35) was the pulmonary hypertension of hyperkinetic type; in all others the arteriolar pulmonary resistance was raised.
RESULTSThe ventilatory and haemodynamic findings are shown in Table I. The average minute ventilation per square meter of body surface (MV/M.2) in all patients was 7 0 ± 1 6 l./min./m.2 which is clearly higher than the normal value of 4-8 ± 1 1 l./min./m.2 in our laboratory by the same procedure. The results in the two groups were as follows:Group 1 (no pulmonary hypertension): 6-4 ±1-4 I./min. /m.2 Group 2 (pulmonary hypertension): 8 5± 1 3 l./min./m.2 The difference between the two groups is statistically highly significant (t = 4 499; p < 0 001).When the minute ventilation was expressed in absolute values the results were nearly the same.
