Dyspnea Due to Vocal Cord Dysfunction and Other Laryngeal Sources

Mark T. O'Hollaren, MD

Disclosures

August 26, 2002

In This Article

Laryngeal Air Flow Limitation Resulting From Abnormal Movement of Laryngeal Structures

Background

The boundaries of the larynx extend from the superior tip of the epiglottis to the cricoid cartilage. The cricoid cartilage serves as the foundation of the larynx, and is actually the only complete cartilaginous ring in the tracheal bronchial tree. The definitive configuration of the larynx is present by 28 weeks of gestation.[4] The true vocal cords serve as a "guardian of the airway." In addition, closing the glottis allows us to have fixation of the thorax, which aids in the mechanisms of heavy lifting using the arms. Finally, motion of the vocal cords allows us to produce vocal sounds for communication, and this process has required the development of a very complex neural control mechanism, which permits precise movements of the vocal cords to produce vocal sounds. Those unfamiliar with the mechanics of voice production feel the process is somewhat simplistic and automatic. However, it is immensely complex and requires the coordination of conceptualized thoughts to be placed in linguistic form, selection of appropriate words, and conversion of these thoughts into appropriate neural impulses. The various laryngeal articulatory structures are then used to produce vocal sounds. While this is taking place, the entire process is monitored using visual, auditory, and proprioceptive systems on an ongoing basis. It is usually when something goes wrong that this complex series of neural and muscular interactions comes to the attention of both the treating physician and the patient.

The respiratory cycle consists of inspiration and expiration, and, in most patients, the glottal opening of the vocal cords is slightly wider on inspiration compared with expiration. In general, however, the average opening of the glottis is fairly constant. This glottic opening is controlled through the medullary respiratory center (via the vagus nerve), which leads to contraction of the posterior cricoarytenoid (PCA) muscle. Contraction of the PCA muscle then leads to opening (abduction) of the vocal cords, which functions to open the glottis and reduce resistance to air flow through the larynx. Contraction of the PCA muscle is also timed with contraction of the diaphragmatic musculature, and is also influenced by variations in both arterial carbon dioxide and oxygen concentrations as well as intrapulmonary pressure.[5]

Of note, it appears that the vocal cords are sensitive to changes in airway caliber as well. Experimentally, histamine-induced bronchospasm may lead to an expiratory narrowing of the vocal cords. Because of this, some feel that the glottis is capable of reflex adjustments in parallel with changes in airway caliber.

Dyspnea resulting from abnormal motion of laryngeal structures has been described in a number of clinical settings, including VCD (also sometimes referred as paradoxical vocal cord motion), vocal cord paralysis, laryngospasm, Meige syndrome, and spastic dysphonia. These disorders may occur in children, adolescents, and adults, and some may have at least a partial functional component. Most do not appear to be under the direct voluntary control of the patient experiencing these symptoms.

As previously mentioned, the vocal cords are normally opened widest during inspiration, and may narrow slightly during expiration in a normal individual. VCD is an phenomenon in which the vocal cords come together (adduct), producing air flow obstruction at the level of the larynx.[6] This abnormal vocal cord motion may produce recurrent wheezing that may imitate asthma, and may be misdiagnosed as asthma for years. If vocal cords close during inspiration, this may lead to stridor, which may be misdiagnosed as an upper airway obstruction of life-threatening severity. The acute presentation, frequently seen in the emergency department, may be dramatic and lead to inappropriate endotracheal intubation, tracheotomy, or recurrent courses of high-dose corticosteroids.[6]

VCD may affect either sex; however, the vast majority of cases described in the literature have been in females. For example, at the National Jewish Center for Respiratory Disease, in the excellent summary by Drs. Newman and Dubester,[6] 37 of 38 patients with VCD without asthma were women. The age of their patients at the time of presentation ranged from 9 to 74 years. However, the most common patient profile involves females between the ages of 20 and 40 years of age, with greater than a high school education and often some affiliation with a health-related field. Approximately 1 of every 4 patients with VCD seen at National Jewish fit this profile.

Clinical presentations of VCD may include wheezing, which may suggest asthma, or stridor, which may suggest upper airway obstruction. The excellent summary by Newman characterizes the clinical and laboratory findings of VCD, as well as therapeutic recommendations.[6] VCD may follow a respiratory infection, although this history is not always given. It is also very common to have VCD occur in the presence of gastroesophageal reflux or significant postnasal drainage. Symptoms may occur with or without exercise, and VCD may occur as an isolated condition or may occur simultaneously in patients with pre-existing asthma.

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