HYPOVENTILATION IN OBESITY*

Abstract

Twenty-six obese subjects were studied; Ventilatory function was assessed in 21, arterial blood gas tensions in 18, blood volume estimations in 16 and the 02 cost of breathing in 25. Clinical history and ventilatory function revealed no evidence of gross lung disease aside from a slight impairment in distribution in 4 patients. Twelve subjects whose arterial blood gas tensions were measured had hypoxia. Four had associated hypercapnia which apparently was due to reduced tidal volumes. Red cell masses per m2 body surface area were increased in both male and female subjects. Plasma volume was increased in the female subjects. The 02 cost of breathing was increased in the obese subjects; it is suggested that this was due to an increase in elastic resistance of the thorax. The individuals who had the highest 02 costs of breathing tended to have the lowest tidal volumes and highest respiratory rates at rest. This may be an example of the selection of an optimum rate and depth of breathing where the least work is done. There appears to be a relationship between the 02 cost of breathing and the arterial CO2 tension in the obese subjects. This is in accordance with the hypothesis that respiratory acidosis is an adaptive mechanism sparing 02-for non-ventilatory work, a rise in CO2 tension being tolerated when the work of breathing is increased.