Despite the fact that the physics of low frequency ultrasound are not fully understood, this study shows that air trapping in COPD can be detected by LFU. We found significant differences in ΔF between healthy subjects and COPD subjects during maximum inspiration and expiration. These differences were already significant at GOLD stage 1 and increased with the severity of COPD. The sensitivity for detecting GOLD stage 1 was 83.3%, for detecting moderate to severe COPD (GOLD 2 and 3) it was 90.9%. Our sensitivity analysis (Table ) showed that these measurements should be obtained during unforced maximum breathing.
Spirometry is required to make the diagnosis of COPD; the presence of a post-bronchodilator FEV1
/FVC < 0.70 confirms the presence of persistent airflow reduction and thus of COPD according to the GOLD guideline recommendations [2
]. Although there is currently insufficient evidence to recommend routine use of low frequency ultrasound, this additional measurement may help to disclose the degree of air trapping in patients with COPD. The method may also be useful in cases where body plethysmography or comparable techniques are unavailable.
In contrast to previous work we found no significant differences in the signal amplitude between COPD patients and healthy subjects [14
]. This may be explained by the subject selection, because Rüter et al.
examined a group of patients with mainly very severe COPD (GOLD stage 4) [14
], while we examined COPD patients with GOLD stages 1 to 3. In principle, however, the present study confirms the previous findings [14
]. As expected, ΔF increased in response to bronchodilation, but these results were not significant. In contrast, bronchodilation as measured by spirometry and by body plethysmography was associated with a significant increase of FEV1
and a significant decrease of airway resistance, respectively. Thus, these conventional measures are more suitable than LFU for assessing bronchodilator responses.
As mentioned above, it is still unclear how low frequency ultrasound is transmitted through the human thorax. Rüter et al.
showed that with increasing air content of the lungs during inspiration the high pass frequency increased while the signal amplitude decreased. It was suggested that sound traveling through the lungs was influenced by differences in lung density [14
]. An important finding in our study was that the typical expiratory signal was received above the abdominal tissue of a healthy person. When placing the sensor above the lower lung border, the signal changed from an expiratory signal with high amplitude and low high-pass frequency during expiration, to an inspiratory signal with lower amplitude and higher high-pass frequency during inspiration. These results can be explained if we assume that the signal is traveling through the abdominal tissue and is attenuated and filtered by the lung, moving into the signal pathway during inspiration. Such a pathway would also explain the dependency on the BMI (Additional file 1
; Suppl. Figure ), because abdominal fat tissue is expected to transmit sound signals well. Thus, the movement of the diaphragm may be the reason for the frequency variability. In COPD hyperinflation of the lungs leads to lowering of the diaphragm and to straightening of the diaphragmatic domes while diaphragmatic movement is reduced [17
]. Rüter et al.
described the expiratory signal of a COPD subject as resembling the inspiratory signal of a healthy person [14
]. Airway obstruction of COPD patients limits their ability to exhale. This would explain why these patients are not able to achieve the expiratory diaphragmatic position of healthy subjects, resulting in an attenuated signal containing higher frequencies. Accordingly, the frequency variability in COPD patients was less pronounced than in healthy subjects and decreased with air trapping.
At present, the LFU method has a number of limitations that need further clarification. It remains uncertain whether the method can be applied to obese patients, as sound transmission through the subcutaneous tissue cannot be excluded. Our studies showed that the signal of subjects with increased body mass index was of higher amplitude than in patients with normal weight. Age, however, does not appear to affect the signal, because a covariate analysis failed to detect age as a factor influencing the LFU signals. However, further studies to define the effect of age and gender are needed. It appears that the necessary degree of cooperation may be less than with conventional FEV1 measurements because meaningful measurements are possible with non-forced maximum expiration. Why the LFU method was even more sensitive with non-forced as opposed to forced expiration breathing is unclear at present; whether this might be explained by the speed and distortion of the chest wall displacement needs to be determined.