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Mechanisms of hyperinflation in asthma
Y Cormier1, R Lecours, C Legris
1Le Centre de Pneumologie, Hôpital Laval, Sainte-Foy, Québec, Canada.
The European Respiratory Journal
|June 1, 1990
Summary
Passive changes in lung volume do not overcome asthma hyperinflation. Persistent inspiratory muscle activity and prolonged expiratory time constants likely cause this condition in asthma patients.
Area of Science:
- Pulmonary Physiology
- Respiratory Medicine
- Asthma Pathophysiology
Background:
- Asthma is characterized by reversible airway obstruction and hyperinflation.
- The mechanisms driving persistent hyperinflation in asthma are not fully understood.
Purpose of the Study:
- To investigate if passive changes in lung volumes can inhibit or overcome asthma-induced hyperinflation.
- To explore the role of inspiratory muscle activity and expiratory time constants in asthma hyperinflation.
Main Methods:
- Mild asthmatic subjects underwent methacholine challenge to induce bronchoconstriction and hyperinflation.
- Functional residual capacity (FRC) and pressures (esophageal, gastric, transdiaphragmatic) were measured using an iron lung with varying extrathoracic pressures.
- Changes in FRC and transdiaphragmatic pressure (Pdi) were analyzed before and after bronchoprovocation.
Main Results:
- Methacholine challenge significantly increased FRC and peak inspiratory Pdi.
- Positive extrathoracic pressures reduced FRC but did not overcome the post-methacholine increase.
- Negative extrathoracic pressures partially reduced the increased peak inspiratory Pdi, but hyperinflation persisted.
Conclusions:
- Passive manipulation of lung volumes does not eliminate or overcome the mechanisms of hyperinflation in asthma.
- Findings support the hypothesis that sustained activity of non-diaphragmatic inspiratory muscles during expiration contributes to hyperinflation.
- A prolonged expiratory time constant is also implicated as a factor in asthma-related hyperinflation.