Fundamentals of Lung Auscultation

Vocal cord dysfunction (VCD) is a syndrome characterized by paroxysms of glottic obstruction due to true vocal cord adduction resulting in symptoms such as dyspnea and noisy breathing. Since first described as a distinct clinical entity in 1983, VCD has inadvertently become a collective term for a variety of clinical presentations due to glottic disorders. Despite an increased understanding of laryngeal function over the past 25 years, VCD remains a poorly understood and characterized entity. Disparities in the literature regarding etiology, pathophysiology, and management may be due to the historic approach to this patient population. Additionally, disorders clearly not due to paroxysms of true vocal cord adduction, such as laryngomalacia, vocal cord paresis, and CNS causes, need to be differentiated from VCD. Although a psychologic origin for VCD has been established, gastroesophageal reflux disease (GERD), nonspecific airway irritants, and exercise have also been associated with intermittent laryngeal obstruction with dyspnea and noisy breathing. VCD has been repeatedly misdiagnosed as asthma; however, the relationship between asthma and VCD is elusive. There are numerous case reports on VCD, but there is a paucity of prospective studies. Following an in-depth review of the medical literature, this article examines the available retrospective and prospective evidence to present an approach for evaluation of VCD including: (1) evaluation of factors associated with VCD, (2) differential diagnosis of movement disorders of the upper airway, and (3) clinical, spirometric, and endoscopic criteria for the diagnosis.

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.