Changes in Ventilatory Muscle Function with Negative Pressure Ventilation in Patients

Posted by James

To the last years, several studies have been devoted to investigating the role of respiratory muscle function in the development of hypercapnia in patients with COPD. Some of these studies have reported that in acutely ill patients, diaphragmatic muscle fatigue is associated with increase in PaC0₂, decrease in maximal inspiratory pressure (MIP), and increase in respiratory frequency (RF) along with a decrease in tidal volume (Vt). Similar ventilatory response, ob­served in patients with stable COPD during loaded breathing, has been interpreted as probably due to poor inspiratory muscle function. In this connection, Roussos has recently hypothesized that in patients with COPD, the rapid and shallow breathing accom­panying chronic hypercapnia may stem from afferents arising from overloaded or fatigued respiratory mus­cles.

A previous article of Rochester et al and more recent articles have shown that negative pressure ventilation (NPV) rests respiratory muscle activity in normal man, while in patients with COPD this may occur or it may not. In patients with chroni­cally stable COPD, NPV also causes PaC0₂ to decrease and MIP to increase. However, until now no study has been designed to assess the following: (1) whether, and to what extent, rest of respiratory muscles may influence the rapid and shallow breathing that accompanies respiratory muscle fatigue in these patients and, (2) the interrelations among breathing pattern, arterial blood gas values, respiratory muscle strength, and phasic suppression of ventilatory muscle activity. The present investiga­tion was carried out to contribute in this field.
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