Abstract
Acute hyperinflation causes the inspiratory muscles to operate at shorter than normal lengths. The ability of these muscles, in particular the diaphragm, to lower intrathoracic pressure is therefore reduced. Skeletal muscles, however, adapt to chronic shortening, and animals models of emphysema have shown that with chronic hyperinflation, the diaphragmatic muscle fibres lose sacromeres. As a result, the force-generating ability of these fibres is relatively preserved. In patients with hyperinflation due to chronic obstructive pulmonary disease, the ability of the diaphragm to generate pressure is also better than anticipated on the basis of hyperinflation alone. However, the diaphragm in these patients is also lower in the chest wall than in healthy subjects. Consequently, even though the neural drive to the muscle is greater than normal, its ability to descend during inspiration is impaired. Its rib cage expanding action is also reduced; in patients with severe hyperinflation, contraction of the diaphragm even produces deflation, rather than expansion, of the rib cage. In such patients, therefore, the ability of the diaphragm to increase lung volume is reduced, and hence the act of breathing is more dependent on the rib cage inspiratory muscles.
