Idiopathic scoliosis. Gas exchange and the age dependence of arterial blood gases

• Published in: The Journal of clinical investigation Vol. 58; no. 4; pp. 825 - 833
• Main Author: Kafer, E R
• Format: Journal Article
• Language: English
• Published: United States 01.10.1976
• Subjects: Adolescent; Adult; Age Factors; Aged; Carbon Dioxide - blood; Child; Female; Humans; Male; Middle Aged; Oxygen - blood; Pulmonary Alveoli - physiopathology; Pulmonary Circulation; Respiration; Respiratory Dead Space; Scoliosis - blood; Scoliosis - pathology; Scoliosis - physiopathology; Tidal Volume; Ventilation-Perfusion Ratio
• ISSN: 0021-9738
• DOI: 10.1172/JCI108535

The aims were to examine the gas exchange and arterial blood gas abnormalities among patients with scoliosis, and the correlation of these abnormalities with age and severity of deformity. Means among 51 patients were as follows: age 25.4 +/- 17.5 yr, angle of scoliosis 80.2 +/- 29.9 (SD), vital capacity 1.94 +/- 0.91 (SD) (i.e. 60.6 +/- 19.2% of predicted), PaO2 85.8 +/- 12.0 (SD), PaCO2 42.4 +/- 8.0, physiological dead space to tidal volume ratio 0.438 +/- 0.074 (SD), and alveolar-arterial oxygen difference breathing air 14.9 +/- 8.9 (SD). Statistically significant correlations were as follows: the PaCO2 and physiological dead space to tidal volume ratio increased with age, and the PaO2 and alveolar ventilation decreased with age. The PaO2, alveolar ventilation, and tidal volume were inversely related to the angle of scoliosis and directly related to the vital capacity, precent predicted vital capacity, and the compliance of the respiratory system. The physiological dead space to tidal volume ratio and the alveolar-arterial oxygen difference were inversely related to the vital capacity, percent predicted vital capacity, and the compliance of the respiratory system. PaCO2 was directly related to the elastance of the respiratory system. We conclude that ventilation-blood flow maldistribution as a result of deformity of the rib cage was the primary abnormality in gas exchange, and that with age there was progressive deterioration in gas exchange. The age-dependent increase in PaCO2 and decrease in alveolar ventilation were due to the increasing physiological dead space to tidal volume ratio and failure of a compensatory increase in ventilation.