Observations placeholder

Rev Port Pneumol. 2006 Jul-Aug;12(4):369-74.
Abnormal respiratory drive in vibroacoustic disease.
Ferreira JR1, Albuquerque e Sousa J, Foreld P, Antunes M, Cardoso S, Alves-Pereira M, Castelo Branco NA.
Author information
 
Abstract
INTRODUCTION:
Central nervous system disorders in workers exposed to low frequency noise (LFN, < 500 Hz, including infrasound) were first observed 25 years ago among aircraft technicians. Concurrently, respiratory pathology was identified in these workers, and later reproduced in LFN-exposed animal models. Today vibroacoustic disease (VAD) is defined as the systemic pathology caused by excessive exposure to LFN. The respiratory tract continues to be under heavy scrutiny in both LFN-exposed humans and animal models and has been confirmed as a major target for LFN-induced damage. Given that both the respiratory and central nervous systems were compromised in these workers, it became pertinent to investigate the status of the neurological control of breathing in VAD patients.

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 CO2, (6% in air) normal individuals present an average seven-fold increase in P0.1 (CO2) 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 P0.1(CO2) 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 P0.1 (CO2) 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 PCO2 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 P0.1 (CO2) index may be a useful clinical indicator for VAD diagnosis and follow-up.
PMID:
16969569