Study objectives: The aim of this study was to measure inspiratory pressure
-generating capacity in patients presenting with acute asthma, as it has be
en suggested that inspiratory muscle fatigue may contribute to breathlessne
ss and acute respiratory failure.
Design: Descriptive study.
Setting: Emergency departments of two inner-city hospitals.
Patients: Fifty-one patients with acute asthma, and 45 patients without res
piratory disease who served as control subjects.
Measurements and results: Maximum inspiratory pressure-generating capacity
was measured soon after presentation by the sniff nasal inspiratory pressur
e (SNIP) method. The mean (SD) SNIP was 110 cm H2O (23 cm H2O) in men with
asthma (mean for control subjects, 126 cm H2O [25 cm H2O]; p < 0.05) and 80
cm H2O [24 cm H2O] in women with asthma (mean for control subjects, 105 cm
H2O (26 cm H2O); p < 0.01). In a second study of simultaneous SNIP and int
rathoracic 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 n
egative than SNIP by approximately 16% in asthmatic patients and by 4% in c
ontrol subjects. Taking account of the likely effect of airways obstruction
on SNIP, the reduction in inspiratory pressure-generating capacity that wa
s observed in these patients with moderately severe acute asthma was minor
and was consistent with the modest hyperinflation observed.
Conclusions: This study did not fmd evidence of inspiratory muscle weakness
or fatigue in patients with moderately severe acute asthma presenting to t
he emergency department.