Effect of isoproterenol on gas exchange during air and oxygen breathing in patients with asthma

Abstract

The effect of isoproterenol on gas exchange during air and oxygen breathing was studied in twenty-five stable asthmatic patients and fourteen normal subjects. Prior to inhalation of isoproterenol the asthmatic subjects had an increased physiologic dead space (V D) (186 ml versus 150 ml), a lower arterial oxygen tension (Pa O2) (77 mm Hg versus 95 mm Hg), a slightly higher diffusing capacity (D L) (34 versus 30 ml/minute/mm Hg) and a normal pulmonary capillary blood volume (V C) (79 ml versus 74 ml). Relief of bronchospasm by isoproterenol inhalation was accompanied by an increase in V D to 253 ml, a decrease in D L to 28 ml/minute/mm Hg, a decrease in V c to 69 ml and a fall in Pa O2 to 69 mm Hg. (In normal subjects there was no significant change in V D, D L, V C or Pa O2.) When the patients breathed 100 per cent oxygen, isoproterenol inhalation increased Pa O2 from 561 to 591 mm Hg. There was a significant positive correlation in alterations in D L, V C and Pa O2 in patients after isoproterenol administration. However, no significant correlation was found between improvement in the indices derived from the forced vital capacity (FVC) compared to changes in D L, V C and Pa O2. Therefore, even though isoproterenol decreases airway obstruction during air breathing, arterial hypoxia may develop. This hypoxemia could not be attributed to hypoventilation or to an increase in the right to left shunt of blood around ventilated alveoli. The changes in V D suggest that hypoxemia resulted from alterations in ventilation-perfusion relationships. The decrease in D L was not large enough to cause hypoxia unless accompanied by profound alterations in diffusion-perfusion distribution. This study indicates that the changes in forced expiratory flow rates cannot be used to identify the asthmatic subject in whom hypoxia will develop after isoproterenol inhalation, but supplementary oxygen will prevent this form of hypoxia.