Vibroacoustic Disease and Respiratory Pathology II - PCO2 Response

摘要

BACKGROUND. Neurological problems in vibroacoustic disease (VAD) patients are characterized by the early onset of degenerative processes, and deregulation of the autonomic nervous system. Simultaneously, studies of low frequency noise- (≤500Hz, including infrasound) (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 and diastolic dysfunction is VAD-specific) have proven to be susceptible to technician-induced subjectivity. In pulmonary functional tests, the P0.1 index is a measure of the suction developed at the mouth 0.1 seconds after the start of inspiration. This initial respiratory drive originates in the involuntary pathway of the neural control of the respiratory function. By rebreathing CO2, normal individuals would present a minimum six-fold increase in the P0.1(CO2) value when compared to normal P0.1. If the neural control of respiration is compromised, then a less-than six-fold increase would be expected. METHODS. Evaluations began in late 2002, and are still ongoing, as is the selection of an appropriate control population. RESULTS. Preliminary data on 22 male VAD patients, average age 50± 8 years (range 36-66 years) had an average P0.1(CO2) value of 25.6 ± 10.8% (normal: ＞60%). DISCUSSION. These data indicate that the autonomic respiratory control in these patients is severely incapacitated. Pending further research, this could be a diagnostic tool for VAD that would not only be non-invasive, reliable, objective and inexpensive, but might also help monitor the progression and follow-up of the disease.