Mechanisms of chronic carbon dioxide retention in patients with obstructive pulmonary disease

Abstract

The investigation was designed to determine the extent to which the arterial carbon dioxide tension (Pa CO 2 ) in patients with obstructive pulmonary disease is under ventilatory control. Thirty male patients, aged thirty-two to fifty-one years, were studied. Hypercapnia occurred almost exclusively in those with the more severe obstruction; only one of ten patients with a 1 second forced expiratory volume (FEV 1) above 1,300 cc. had hypercapnia during exercise, whereas fifteen of nineteen patients with an FEV 1 below 1,300 cc. had hypercapnia during exercise. Total minute ventilation during exercise was normal or increased in all patients, and there was no relationship between minute ventilation either at rest or during exercise and Pa CO 2 . There was a correlation between values for Pa CO 2 obtained during exercise and the ratio of physiological dead space to tidal volume (R = 0.607, p < 0.001). Voluntary hyperventilation was usually ineffective in producing substantial lowering of Pa CO 2 and often resulted in a further increase in Pa CO 2 ; this was especially true during exercise. Two mechanisms accounted for this: (1) ineffectiveness of the ventilatory process so that increases in minute ventilation produced no change or actual decreases in alveolar ventilation, and (2) even with increases in alveolarventilation, there were proportional increases in carbon dioxide output, which prevented a fall in Pa CO 2 . Thus chronic hypercapnia in patients with obstructive pulmonary disease is not due to overall underventilation. The disease state requires an effective increase in ventilation for the maintenance of a normal Pa CO 2 . Subjects with hypercapnia appear unable to accomplish this increase without an excessive dead space ventilation or without an excessive increase in the carbon dioxide production of the respiratory muscles.