Abnormal respiratory drive in vibroacoustic disease

Abstract Introduction Central nervous system disorders in workers exposed to low frequency noise (LFN, Methods The P- 0.1 value, a measure of the suction pressure developed at the mouth 0.1 seconds after the start of inspiration, depends on the respiratory centres and the autonomic nervous system pathway of the neural control of respiratory function. By rebreathing CO 2 , (6% in air) normal individuals present an average seven-fold increase in P 0.1 (CO 2 ) as compared to basal P- 0.1 . Twenty-two male VAD patients (ave. age 50.5 ± 8.5 years, range: 36-66 years) underwent the P 0.1 (CO 2 ) index respiratory drive tests, as well as standard pulmonary function tests. Seven individuals (ave. age 42.4 ± 14 years, range: 25- 61 years) with reduced LFN exposure served as controls. Results Pulmonary function tests were normal in both VAD patients and controls. The P 0.1 (CO 2 ) index was below average value in VAD patients (average: 22.9%) while it presented normal values in the control group (average >60%). Discussion In the involuntary response to increased PCO 2 levels, central chemoreceptors are responsible for 70% of the ventilatory stimulus. In VAD patients, this dysfunction may originate in the brainstem. This is corroborated by the fact that VAD patients register abnormal values for auditory brainstem evoked potentials, and disclose lesions with magnetic resonance imaging. The neurological control of breathing is compromised in VAD patients. The P 0.1 (CO 2 ) index may be a useful clinical indicator for VAD diagnosis and follow-up.