Inspiratory muscle strength in acute asthma

The aim of this study was to measure inspiratory pressure-generating capacity in patients presenting with acute asthma, as it has been suggested that inspiratory muscle fatigue may contribute to breathlessness and acute respiratory failure.

Descriptive study.

Emergency departments of two inner-city hospitals.

Fifty-one patients with acute asthma, and 45 patients without respiratory disease who served as control subjects.

Maximum inspiratory pressure-generating capacity was measured soon after presentation by the sniff nasal inspiratory pressure (SNIP) method. The mean (SD) SNIP was 110 cm H(2)O (23 cm H(2)O) in men with asthma (mean for control subjects, 126 cm H(2)O [25 cm H(2)O]; p < 0.05) and 80 cm H(2)O [24 cm H(2)O] in women with asthma (mean for control subjects, 105 cm H(2)O (26 cm H(2)O); p < 0.01). In a second study of simultaneous SNIP and intrathoracic pressure measurements in a group of patients with acute asthma (n = 10) and control subjects (n = 11), the effect of airways obstruction on SNIP was assessed. The measurement of sniff esophageal pressure was more negative than SNIP by approximately 16% in asthmatic patients and by 4% in control subjects. Taking account of the likely effect of airways obstruction on SNIP, the reduction in inspiratory pressure-generating capacity that was observed in these patients with moderately severe acute asthma was minor and was consistent with the modest hyperinflation observed.

This study did not find evidence of inspiratory muscle weakness or fatigue in patients with moderately severe acute asthma presenting to the emergency department.