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Thorax 2000;55:1016-1022; doi:10.1136/thorax.55.12.1016
Copyright © 2000 BMJ Publishing Group Ltd & British Thoracic Society.
Thorax 2000;55:1016-1022 ( December )

Hyperventilation and asymptomatic chronic asthma

C A Osborne, B J O'Connor, A Lewis, V Kanabar, W N Gardner

Department of Respiratory Medicine and Allergy, Guy's, King's and St Thomas' School of Medicine, King's Denmark Hill Campus, London SE5 9PJ, UK

Correspondence to: Dr W N Gardner william.gardner{at}kcl.ac.uk

Received 28 February 2000; Returned to authors 3 May 2000; Revised version received 22 August 2000; Accepted for publication 23 August 2000

BACKGROUND---We have consistently argued that mild asthma is an important underlying aetiological factor in patients with severe symptomatic hyperventilation. While hyperventilation has been demonstrated in acute asthma, there have been few studies in mild chronic asthma, and mechanisms are uncertain.
METHODS---Twenty three currently asymptomatic chronically asthmatic patients (occasional use of bronchodilators, normal lung function, hyperresponsive to methacholine) were studied and 17 matched normal subjects acted as controls. Ventilation, pattern of breathing, arterial carbon dioxide and oxygen tensions (PaCO2, PaO2), end tidal PCO2 (PETCO2), standard lung function, airway responsiveness to methacholine, airway inflammation assessed by eosinophils in induced sputum, and psychiatric morbidity (Spielberger STAI-Y and Beck Depression Inventory) were measured.
RESULTS---Despite the absence of current asthmatic symptoms, no clinical evidence of hyperventilation, and normal lung function in the patients with asthma, PaCO2 and PETCO2 were significantly (p<0.01) lower in the patients than in the control group (mean (SD) PaCO2 4.96 (0.43) kPa for patients versus 5.27 (0.38) kPa for controls (mean difference 0.31 kPa, 95% confidence interval (CI) 0.06 to 0.56, p<0.02)). PETCO2 was very similar to PaCO2 in both groups (mean (SD) PETCO2 4.89 (0.47) kPa for the patients and 5.28 (0.40) for the controls (mean difference 0.39 kPa, 95% CI 0.12 to 0.66, p<0.01)). There was no significant difference in ventilation or respiratory pattern between the two groups. The reduced PaCO2 in the asthmatic patients correlated significantly with the concentration of methacholine provoking a fall in FEV1 of more than 20% (PC20) (r = 0.56, p<0.01) but not with any aspect of lung function, eosinophil count, or anxiety/depression.
CONCLUSION---Mild asymptomatic asthma is not associated with clinically significant hyperventilation but is associated with a significant reduction in both arterial and end tidal PCO2 which relates to airway hyperresponsiveness rather than to the degree of airway obstruction or mucosal inflammation. Anxiety and depression appear not to be implicated.


Keywords: breathing pattern; hypocapnia; carbon dioxide; hyperventilation syndrome; asthma


© 2000 by Thorax

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