Exercise induced dyspnoea: if not asthma, then what?

The report by Seear et al found that most children referred to their clinic with a history of exercise induced asthma (EIA) did not have asthma.¹ These investigators conclude that the majority of exercise associated respiratory complaints can be diagnosed and managed without the need for exercise testing. The accompanying editorial concurs with that view.² Our own study, recently published, is supportive of the overdiagnosis of asthma as a cause of exercise induced dyspnoea (EID).³ However, I would argue against the conclusion that formal exercise testing is not indicated. In fact, our experience showed the value of full cardiopulmonary evaluation with breath‐by‐breath analysis of oxygen consumption and carbon dioxide production for such children during exercise sufficient to reproduce their symptoms.

By reproducing EID in 117 patients, most of whom had been previously diagnosed and treated for asthma, while continuously monitoring their cardiopulmonary physiology, we identified only 11 who had EIA during reproduction of their EID. Fifteen had flattening of the inspiratory portion of the flow‐volume loop at the time of reproduction of symptoms. Direct visualisation with a flexible laryngoscope while symptoms were present distinguished two who had exercise induced laryngomalacia from those with vocal cord dysfunction. There were other patients who had what sounded like inspiratory stridor at very high minute ventilation but did not have evidence for upper airway obstruction. They simply moved sufficient air through a normal variant airway that an inspiratory sound could be reproduced during maximal exercise. We also identified 15 who, when their EID was reproduced, attained their maximal minute ventilation with a decreased maximal tidal volume and abnormally high respiratory rate consistent with a component of chest wall restriction not apparent at rest. One patient only had exercise induced hyperventilation, a phenomenon we have previously reported in others.⁴ Supraventricular tachycardia demonstrable by ECG was identified in a well conditioned highly competitive teenage athlete whose heart rate jumped suddenly to 220 during maximal exercise in association with his EID. He underwent a successful ablation by our cardiac electophysiologist which completely eliminated this young athlete's EID, enabling him to complete a full basketball game without having to repeatedly stop to recover. Since our publication, we have identified another teenager whose EID was associated with supraventricular tachycardia, also only present during vigorous exercise. Both of these adolescents had been previously treated unsuccessfully for EIA. Of the 117 in whom we reproduced their EID during the treadmill exercise, 74 had only normal physiological exercise limitation, with cardiovascular conditioning among them about equally divided between poor, average, and above average cardiovascular conditioning.

Our experience is that simply identifying the absence of EIA is not sufficient. Even for the 74 with no physiological abnormality, we were able to counsel those with poor cardiovascular conditioning regarding the means to improve exercise ability and could even counsel those with excellent cardiovascular conditioning about the need for training to learn how to manage normal exercise limitation. Moreover, since dyspnoea from any cause is anxiety producing, identifying the cause of the EID and providing recommendations for a potential solution relieves that anxiety component which was likely to be a factor in seeking medical care and receiving inappropriate treatment in the first place.

In the study by Saeer et al, one wonders if all eight children identified as having EIA actually had asthma as the cause of their EID since the diagnosis was based on an FEV₁ decrease ⩾10% but <15% in six, decreases which may be within normal limits for non‐asthmatics.⁵ In contrast to the 21% of children with no diagnosis for their EID, we were able to identify the cause of EID in all of our patients in whom full cardiopulmonary monitoring was performed in association with sufficient exercise to reproduce their symptoms.

Thus, while we certainly agree with Seear et al and the accompanying editorial that EIA is overdiagnosed, our experience would argue for exercise testing that reproduces the symptoms of EID during continuous cardiopulmonary monitoring for those whose history is otherwise atypical for asthma.