Mechanisms and consequences of hyperinflation.

The mechanisms and pathophysiological consequences of hyper inflation are complex and not fully elucidated [1). In the present issue of the journal, WHEATLEY et al. [2] and CoRMJER e1 al. [3) provide additional data contributing to our understanding of these aspects of hyperinflation in induced bronchoconsLriction. One of the mechanisms of hyperinflation may be changes in the static equilibrium between lung and chest wall as a consequence of a loss of elastic recoil of the lung and a shift of the static lung volume-pressure curve upward and to the left [4), or of a "resetting" of the passive elastic characteristics of the chest wall [5). However, in conditions of bronchoconstriction, the hyperinflation is apparently determined mainly by dynamic factors [6]. The most important of these is the increased airway resistance with prolonged mechanical expiratory time constants and, thus, slow and incomplete lung emptying [1, 6]. Another factor is a pers is tin g inspiratory muscle activity during expiration [7-1 0]. This is believed to be accessory and intercostal in nature rather Lhan diaphragmatic [8, 9). although elec trical activity has also been demonstrated in the lauer muscle (10]. Furthermore, glottic constriction during expiration [11] and enhanced airway closure [12J have been demonstrated to accompany bronchoconstriction and have been suggested to contribute also to the hyperinDation. Finally. chronic adaptations of inspiratory muscles to shorter operating lengths and to permanently increased loads may occur in chronic obstructive pulmonary disease (COPD) [6] as occurs in experimentally induced emphysema in animals [13), and may thus also intervene in the hyperinflation. In their present paper, CoRMIER et al. [3] have tried to shed more light on the mechanisms determining hyperinflation by investigating the extenr to wh.ich the hyperinflation may be influenced by changes in the passive clastic loads, induced by applying extrathoracic pressures on asthmatic subjects lying inside an iron lung. After provoking a decrease in forced expiratory volume in one second (FEY) of about 40% and an increase in functional residual capacity (FRC) of about 30% by methacholine inhalation they find that, while negative cxtrathoracic pressures lead to a funhcr lung expansion, positive pressures can reduce the hyperinflation only from about 730 ml above the prc-challenge level to a lower plateau level of about 450 ml above the control FRC. They conclude that these data support the hypothesis that