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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