Thus, the ventilatory pattern adopted by these asthmatic subjects in response to bronchoconstriction is probably optimal under the circumstances. The ventilatory pattern response to inhaled histamine is believed to be neurally mediated via airway irritant receptors; hypoxemia itself increases respiratory frequency but usually without any decrease in Vt. The ventilatory pattern changes observed after bronchoconstriction in the present study were similar to those seen in chronic stable asthma. review
A curious feature of the present study is the finding that alveolar ventilation did not increase in these asthmatic subjects with induced bronchoconstriction. In this regard, these subjects responded in a similar manner to patients with chronic bronchitis and emphysema, who respond to methacholine-induced bronchoconstriction with alveolar hypoventilation, which is in contrast to the hyperventilation occurring with spontaneous bronchoconstriction in asthmatics. This could be a function of the degree of bronchoconstriction, the length of time over which it occurred, or of the bronchoconstrictor stimulus itself. Further work is necessary to elucidate this.
The present study indicates that there may be a profound decrease in arterial Po2 following histamine challenge even in very mild, stable asthma. The clinical implications of the present study are that bronchoconstrictor challenge should be undertaken with caution in patients with decreased resting Pa02 and that the arterial Po2 or oxygen saturation should probably be monitored in these subjects; it may be necessary to give supplemental oxygen in some patients during a bronchoconstrictor challenge. The results of the present study indicate that the decrease in Pa02 is primarily due to an increase in the physiologic dead space, which is also influenced by a marked change in ventilatory pattern.