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(Chest. 2001;120:757-764.)
© 2001 American College of Chest Physicians

Inspiratory Muscle Strength in Acute Asthma*

Ian M. Stell, MBBS; Michael I. Polkey, PhD; P. John Rees, MD; Malcolm Green, MD and John Moxham, MD

* From the Departments of Accident & Emergency Medicine (Dr. Stell) and Respiratory Medicine (Drs. Polkey and Moxham), King’s College Hospital, London, UK; the Department of Respiratory Medicine (Dr. Rees), Guy’s Hospital, London, UK; and the Department of Respiratory Medicine (Dr. Green), The Royal Brompton Hospital, London, UK.

Correspondence to: Ian M. Stell, MBBS, Accident & Emergency Department, Bromley Hospital, Cromwell Avenue, Bromley, Kent, BR2 9AJ UK; e-mail ian.stell@bromleyh_tr.sthames.nhs.uk

Study objectives: 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.

Design: Descriptive study.

Setting: Emergency departments of two inner-city hospitals.

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

Measurements and results: 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 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 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.

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

Key Words: asthma • respiratory insufficiency • respiratory muscles • muscle fatigue




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