Respiratory sounds (RSs) recorded from the chest and trachea are nowadays being electronically analysed by many investigators with a view to (i) determining the mechanisms of their production, and (ii) to develop automated diagnostic systems based on RS analysis, that objectively categorise RS as being associated with health or respiratory diseases. However, one problem that hampers this type of research is that almost every RS investigation team uses different equipment, protocols and analysis methods which, to varying degrees, makes inter-investigator results difficult to compare. The review first discusses the many variables involved in RS recording and analysis, and the different approaches used by different investigators, to highlight this problem and its consequences. Secondly, although the review cannot propose immediately acceptable guidelines and standards for RS analysis, it proposes a 'seed' set of guidelines that are 'up for discussion' between investigators in the field, the final goal being to inject a degree of standardisation in equipment and methods that are acceptable to all involved.

Tracheal breath sounds (TBSs) were analysed in 12 normal adult subjects at the air flow levels of 1.6, 2.1 and 2.6 litres-1, using a low-resistance flow transducer, and at an estimated flow of 2.1 litres-1 without the flow transducer. The major findings were that the TBSs were significantly distorted by the flow transducer, but were independent of air flow. We therefore conclude that true TBSs can only really be recorded when an oral flow transducer is not used. The within-subject reproducibility of TBS was relatively good, while the cross-subject comparison of TBS showed that each subject produced their own unique spectral pattern, although the TBSs of normal subjects fall in a common frequency range. Also, inspiratory sounds were significantly lower in peak frequency than expiratory TBSs.

Expired and inspired tracheal breathing sounds (BS) were recorded from 10 normal subjects and 8 patients with respiratory diseases, including bronchial asthma, sarcoidosis, fibrosing lung disease, chronic bronchitis, and radiation pneumonitis. Frequency spectra were generated using Fast Fourier Transform (FFT), and we observed considerable differences between BS spectra of normal subjects and patients. The frequency of peak amplitude and mean frequency of the BS spectra of patients were significantly higher than those of normal subjects. Spectral features were extracted by dividing each spectra into equal frequency bands--each feature being the mean amplitude of each FFT element within a frequency band. We used Principal Component Analysis to compare spectral feature sets and found a clear separation between normal and abnormal tracheal BS for 10, 20, and 40 features/spectra. We conclude that Principal Component Analysis of BS could become a new method of diagnosing respiratory disease in an automated fashion.

We review some of the evidence that supports the existence of psychosomatic triggers to bronchospasm in asthmatics, and hypothesize that it may also be possible to consciously reverse bronchospasm using trachea-noise biofeedback. We precipitated significant levels of bronchospasm in 16 asthmatics using exercise or eucapnic-hyperventilation challenges on five occasions, and administered four different treatments and a no-treatment control. The treatments were trachea-noise biofeedback (TNBF), wrong-information TNBF, an inhaled adrenergic bronchodilator, and a placebo inhaler, all given double blind. Half of the subjects had 3 training days in the use of the TNBF device before study. Our results show that TNBF, in the trained subjects only, is associated with a detectable, but not statistically significant, increase in the rate of recovery from bronchospasm over that found with no treatment. We conclude that, although asthmatics seem to have a strong ability to consciously induce bronchospasm, conscious reversal of a full asthma attack using TNBF is limited. Despite contrary conclusions by other investigators, we believe that this study demonstrated little TNBF-assisted recovery from bronchospasm. We suggest that this is because its effect may be inhibited by humoral mechanisms that sustain the attack, but we believe further work is required to support this.

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