Abstract: Poster Presentations |

Respiratory Drive in Vibroacoustic Disease FREE TO VIEW

José Reis Ferreira, MD; Carla P. Mendes, MD; Marco Antunes, BSc; Mariana Alves-Pereira, PhD Candidate; Nuno Castelo Branco, MD
Author and Funding Information

Portuguese Air Force Hospital, Lisbon, Portugal


Chest. 2003;124(4_MeetingAbstracts):214S. doi:10.1378/chest.124.4_MeetingAbstracts.214S
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PURPOSE:  Vibroacoustic disease (VAD) is caused by long-term exposure (years) to low frequency noise (LFN) [≤500 Hz, including infrasound]. Neurological problems in VAD patients are characterized by the early onset of degenerative processes, and deregulation of the autonomic nervous system. Simultaneously, studies of LFN-exposed rats show that the respiratory system is a target for this agent of disease. Taken together, this information led to speculation regarding the status of the respiratory reflex response in these patients. Concurrently, there is an ongoing search for a non-invasive, objective and inexpensive diagnostic test for VAD, since echocardiograms (thickening of cardiac structures in the absence of an inflammatory process is the hallmark of VAD) have proven to be susceptible to technician-induced subjectivity. Pulmonary functional tests might be eligible for the role.

METHODS:  Thirty male VAD patients and 20 age-matched controls (range 38-63 years) performed pulmonary function tests including the following parameters: forced expiratory volume in the first second of expiration, vital capacity (VC), peak expiratory flow, and maximal expiratory flows at 50% and 25% of VC, airway resistance, and P0.1(CO2) index. Individuals with thickened cardiac structures, as viewed through echocardiography, and/or with known neurological disorders were excluded from the control population.

RESULTS:  When compared to controls, no difference in any of the pulmonary parameters were identified, with the dramatic exception of the P0.1(CO2) index (range 8 -58%; norm: >70%) [p < 0.05].CONCLUSIONS: These data indicate that the status of the respiratory reflex response in VAD patients is severely decreased. Taken together with the already described neurological disorders associated with VAD, a new understanding of the possible pathways of LFN-induced lesions may emerge. More immediately, it is possible that the P0.1(CO2) index might be the desired non-invasive, objective and inexpensive test for VAD diagnosis and clinical follow-up.

CLINICAL IMPLICATIONS:  The P0.1(CO2) index may be the diagnostic tool of choice for diagnosing and monitoring VAD.

DISCLOSURE:  J. Reis Ferreira, None.

Wednesday, October 29, 2003

12:30 PM - 2:00 PM




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