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Published ahead of print on April 1, 2004, doi:10.1164/rccm.200207-720OC

Am. J. Respir. Crit. Care Med., Volume 170, Number 2, July 2004, 118-125

A more recent version of this article appeared on July 15, 2004
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Submitted on July 21, 2002
Accepted on March 31, 2004

Ventilatory Responses to CO2 Inhalation, Hypoxia and Exercise in Idiopathic Hyperventilation

Sandy Jack, Harry B Rossiter, Michael G Pearson, Susan A Ward, Christopher J Warburton*, and Brian J Whipp

* To whom correspondence should be addressed. E-mail: cjwarby{at}liverpool.ac.uk.

Idiopathic hyperventilation is a poorly understood condition of sustained hypocapnia and controversial etiology. While behavioral/emotional factors may contribute, it is uncertain whether: chemosensitivity is altered; hyperventilation is maintained during exercise; and the associated breathlessness reflects the hyperventilation. In 39 patients with idiopathic hyperventilation and 23 controls, we described: ventilatory responses to isocapnic-hypoxia, hyperoxic-hypercapnia and exercise; breath-hold tolerance; breathlessness; psychological status. Patients demonstrated hyperventilation at rest, with hypocapnia (28±3.8 mm Hg), a normal (slightly alkaline) pHa and [H+]a, and a significant base excess (-4.5±2.7 mEq/l); consistent with compensated respiratory alkalosis. Hyperventilation was sustained during exercise, despite hyperoxic-hypercapnic ventilatory responsiveness being normal and isocapnic-hypoxic ventilatory responsiveness being low relative to control (but exceeding control (2.4±1.0 vs. 1.6±0.5 l/min/%; P<0.05) with acute restoration to normocapnia). Hyperventilation was maintained during exercise, at the resting CO2 "set-point". Relative to control, breath-hold tolerance was attenuated, and dyspnea during exercise was significantly greater and not simply ascribable to the high ventilation. These observations suggest that patients with idiopathic hyperventilation have a sustained hyperventilatory and dyspneic drive that, while not attributable to central chemosensitivity, may possibly have peripheral chemoreflex contributions. The nature and etiology of this chronic hyperventilatory drive remain unclear.
Key words: Peripheral chemoreflex; Central chemoreflex; Dyspnea; Breath-holding




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