Vyshedskiy Andrey, Alhashem Ruqayyah M, Paciej Rozanne, Ebril Margo, Rudman Inna, Fredberg Jeffrey J, Murphy Raymond
Brigham and Women's/Faulkner Hospitals, Boston University, and Harvard School of Public Health, Boston, MA.
Brigham and Women's/Faulkner Hospitals, Boston University, and Harvard School of Public Health, Boston, MA.
Chest. 2009 Jan;135(1):156-164. doi: 10.1378/chest.07-1562. Epub 2008 Aug 8.
Although crackles are frequently heard on auscultation of the chest of patients with common cardiopulmonary disorders, the mechanism of production of these sounds is inadequately understood. The goal of this research was to gain insights into the mechanism of crackle generation by systematic examination of the relationship between inspiratory and expiratory crackle characteristics.
Patients with a significant number of both inspiratory and expiratory crackles were examined using a multichannel lung sound analyzer. These patients included 37 with pneumonia, 5 with heart failure, and 13 with interstitial fibrosis. Multiple crackle characteristics were calculated for each crackle, including frequency, amplitude, crackle transmission coefficient, and crackle polarity.
Spectral, temporal, and spatial characteristics of expiratory and inspiratory crackles in these patients were found to be similar, but two characteristics were strikingly different: crackle numbers and crackle polarities. Inspiratory crackles were almost twice as numerous as expiratory crackles (n = 3,308 vs 1,841) and had predominately negative polarity (76% of inspiratory crackles vs 31% of expiratory crackles).
These observations are quantitatively consistent with the so-called stress-relaxation quadrupole hypothesis of crackle generation. This hypothesis holds that expiratory crackles are caused by sudden airway closure events that are similar in mechanism but opposite in sign and far less energetic than the explosive opening events that generate inspiratory crackles. We conclude that the most likely mechanism of crackle generation is sudden airway closing during expiration and sudden airway reopening during inspiration.
尽管在患有常见心肺疾病的患者胸部听诊时经常能听到啰音，但对这些声音的产生机制了解不足。本研究的目的是通过系统检查吸气性和呼气性啰音特征之间的关系，深入了解啰音产生的机制。
使用多通道肺音分析仪对同时存在大量吸气性和呼气性啰音的患者进行检查。这些患者包括37例肺炎患者、5例心力衰竭患者和13例间质性纤维化患者。计算每个啰音的多个特征，包括频率、幅度、啰音传导系数和啰音极性。
发现这些患者呼气性和吸气性啰音的频谱、时间和空间特征相似，但有两个特征明显不同：啰音数量和啰音极性。吸气性啰音的数量几乎是呼气性啰音的两倍（3308个对1841个），且主要为负极性（76%的吸气性啰音对31%的呼气性啰音）。
这些观察结果在数量上与所谓的啰音产生的应力松弛四极子假说一致。该假说认为，呼气性啰音是由突然的气道关闭事件引起的，其机制相似，但符号相反，且比产生吸气性啰音的爆发性开放事件能量小得多。我们得出结论，啰音产生的最可能机制是呼气时气道突然关闭和吸气时气道突然重新开放。
