Hyperventilation and asymptomatic chronic asthma

Background-We have consistently argued that mild asthma is an important und erlying aetiological factor in patients with severe symptomatic hyperventil ation. 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 t o methacholine) were studied and 17 matched normal subjects acted as contro ls. Ventilation, pattern of breathing, arterial carbon dioxide and oxygen t ensions (Paco(2), Pao(2)), end tidal Pco(2) (PETCO2), Standard lung functio n, airway responsiveness to methacholine, airway inflammation assessed by e osinophils 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 evid ence of hyperventilation, and normal lung function in the patients with ast hma, Paco(2) and PETCO2 were significantly (p<0.01) lower in the patients t han in control group (mean (SD) Paco(2) 4.96 (0.43) kPa for patients versus 5.27 (0.38) kPa for controls (mean difference 0.31 kPa, 95% confidence int erval (CI) 0.06 to 0.56, p<0.02)). PETCO2 was very similar to Paco(2) in bo th 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 Paco(2) in the asthmatic patients corr elated significantly with the concentration of methacholine provoking a fal l in FEV1 of more than 20% (PC20) (r = 0.56, p<0.01) but not with any aspec t of lung function, eosinophil count, or anxiety/depression. Conclusion-Mild asymptomatic asthma is not associated with clinically signi ficant hyperventilation but is associated with a significant reduction in b oth arterial and end tidal Pco(2) which relates to airway hyperresponsivene ss rather than to the degree of airway obstruction or mucosal inflammation. Anxiety and depression appear not to be implicated.