All That Wheezes Is Not Asthma: Diagnosing the Mimics

Especially when the standard therapy for asthma has failed to produce improvement, the clinician should be alert to signs of other conditions that can closely resemble asthma, ranging from congestive heart failure to vocal cord dysfunction.

By Francisco J. Soto, MD, and Kalpalatha K. Guntupalli, MD

Dr. Soto is clinical instructor and Dr. Guntupalli is professor of medicine in the Pulmonary/Critical Care Division at Baylor College of Medicine in Houston. Dr. Guntupalli is also associate chief of medicine, chief of the pulmonary/critical care unit, and director of the medical intensive care unit at Ben Taub General Hospital in Houston.

Wheezing, or high-pitched adventitious sounds superimposed on the normal sounds of breathing, occurs when air flows rapidly through narrowed bronchi. Clinically, it should be viewed as a nonspecific manifestation of airway obstruction. Asthma is its most common cause, especially when the wheezing is episodic and the patient is young, but other medical conditions that can be mistaken for asthma should be considered. In particular, when the standard therapy for asthma has failed to produce improvement, a differential diagnosis needs to be undertaken or revisited.

In this article, we will discuss a variety of conditions that can be labeled as asthma, leading not only to delayed diagnosis but also to inappropriate treatment. The differential diagnosis of a patient with wheezing should also include diseases that affect the upper airways. The list of conditions is long, and we will focus only on the more common conditions that the clinician is likely to encounter.

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Preliminary Indications in the History and Physical Examination

A number of features in the history are helpful in establishing the etiology of wheezing (see table below). In children, the clinician should suspect foreign body aspiration, especially if the symptoms started rather suddenly; congenital heart disease; and cystic fibrosis, if a patient has a history of gastrointestinal or upper airway symptoms. Adults may also present with wheezing due to foreign body aspiration. Up to a third of adult patients with foreign body aspiration do not recall choking episodes. First-time wheezing in an older adult, especially a smoker, should alert the physician to the possibility of lung cancer. Both malignant lesions and benign tumors such as squamous papilloma, leiomyoma, bronchial cyst adenoma, or carcinoid tumor can present with hoarseness, hemoptysis, inspiratory stridor or wheezing, but the benign airway tumors are rare. Sudden onset of wheezing in adults might be due to left ventricular failure ("cardiac asthma"), pulmonary embolism, aspiration pneumonitis, or a foreign body. Other clues such as the timing of symptoms (wheezing late at night, for example) and the presence of orthopnea, dyspnea on exertion, peripheral edema, or paroxysmal nocturnal dyspnea are also helpful.

Disorders Associated with Wheezing According to Age, Onset, and Course Age Infants and children Congenital anomalies Bronchopulmonary dysplasia Bronchomalacia Vascular rings Cystic fibrosis Foreign body aspiration Adults Asthma Chronic obstructive pulmonary disease (COPD) Congestive heart failure (CHF) Primary endobronchial tumors Endobronchial metastasis (from colon, breast, melanoma, kidney, pancreas) Onset Acute Asthma CHF Pneumonia Pulmonary embolism Anaphylaxis Aspiration syndromes Foreign body aspiration Insidious Bronchogenic carcinoma Tracheal tumor Endobronchial metastasis CHF Course Intermittent Aspiration syndromes COPD Asthma CHF Carcinoid syndrome Vocal cord dysfunction Persistent Endobronchial tumor Tracheal stenosis Bilateral vocal cord paralysis Asthma Churg-Strauss syndrome Progressive COPD Tumors Pulmonary infiltrates/eosinophilia syndromes

A knowledge of the anatomy of the upper airway‹the air-conducting passages from the nose or mouth to the main carina‹is helpful in understanding the pathophysiology of some of the asthma mimics. The upper airway comprises three sectors: the anatomic spaces around the mouth and nose that can be potentially occupied (as in Ludwig's angina), the larynx, and the trachea. The larynx, which extends from the root of the tongue to the trachea, consists of the supraglottic larynx (epiglottis, aryepiglottic folds, and false vocal cords), the glottis (structures at the level of the vocal cords, including arytenoid cartilages), and the subglottis (the 1.5- to 2-cm segment of the airway surrounded by the cricoid cartilage). The trachea (10 to 13 cm long and 13 to 25 mm in coronal diameter in men, 10 to 21 mm in women) is conceptually divided in two by the thoracic inlet. The extrathoracic trachea is 2 to 4 cm long, extending from the lower edge of the cricoid cartilage to the thoracic inlet, and is located 1 to 3 cm above the suprasternal notch. The intrathoracic trachea extends 6 to 9 cm from the thoracic inlet to the main carina.

In the wheezing patient, characteristics of the voice may be helpful in pointing to a diagnosis. Changes in the voice, such as the so-called hot potato voice (the patient talks as if he had a hot potato in his mouth) associated with oral abscess and Ludwig's angina, are helpful when trying to determine the etiology or location of the obstruction (see table below).

Vocal Attributes and Associated Airway Problems Symptom Disorder Hoarseness Unilateral vocal cord paralysis Croup Muffled voice Supraglottic process "Hot potato" voice Oral abcess Ludwig's angina "Barking" cough Laryngotracheobronchitis No hoarseness Epiglottitis Drooling, dysphagia Epiglottitis Fever without cough Epiglottitis Monotone, hurried sentences, inspiratory pause Bilateral vocal cord paralysis Suppressed laughter or cough Bilateral vocal cord paralysis

On inspection, thyroidectomy or tracheostomy scars should alert the examiner to consider vocal cord damage or tracheal/laryngeal stenosis. Jugular venous distention might be associated with congestive heart failure and cardiac asthma. In a patient who looks septic, neck swelling should alert the clinician to a possible deep space infection, such as Ludwig's angina. The presence of facial flushing (carcinoid tumor), vasculitic skin lesions (Churg-Strauss), or venous congestion (venous thrombosis) in the physical exam also contributes to the assessment of wheezing. The presence of clubbing in a young patient with wheezing raises the possibility of underlying congenital heart disease or bronchiectasis secondary to cystic fibrosis. In an older patient, clubbing may be associated with bronchogenic carcinoma. Any evidence of residual neurologic deficit in a patient whose gag reflex is absent due to previous strokes indicates increased risk for recurrent aspiration.

On palpation, cervical or axillary lymphadenopathy may be related to an intrathoracic process, such as bronchogenic carcinoma or lymphoma. Thyromegaly or a neck mass may be responsible for the compression of the upper airway.

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Interpreting Chest Sounds

On auscultation, the clinician should listen for signs of cardiac disease, including the presence of a loud second heart sound, a third heart sound, or a murmur, which may suggest pulmonary hypertension with venous thromboembolic disease, congestive heart failure, or valvular heart disease. The tone, timing, and location of the wheezing provide additional clues (see table below).

Any monotonal wheezing, whether inspiratory, expiratory, or both, may be indicative of structural or functional upper airway disease. Auscultation during a wheezing episode can be very helpful in further characterizing the patient's breathing problem. However, the findings may vary from episode to episode. Also, while the timing and apparent location of wheezing may be significant, even the most localized obstruction can produce diffuse bilateral sounds. (See table below, for possible causes of unilateral wheezing.) The typical wheezing during expiration implies bronchiolar disease, either primary (due to structural change) or secondary (as in air trapping), both of which can be seen in asthma. The patient with asthma may wheeze during inspiration as well.

Causes of Unilateral Wheezing Foreign body Airway stenosis Bronchomalacia Airway compression Vascular enlargement Lymphadenopathy Cyst Neoplasm (external compression) Endobronchial tumors Primary malignancy (bronchogenic carcinoma) Benign tumors Bronchial cyst adnenoma Squamous papilloma Leiomyoma Carcinoid (might behave aggressively) Malignant metastasis from breast, colon, rectum, pancreas, kidney, thyroid, or skin

Certain auscultatory features help to differentiate wheezing from stridor. "Stridor" is a Latin word meaning a hiss, grating, creaking, whistle, or shriek. In asthma, wheezing is usually diffuse and polyphonic, occurring prominently during expiration. Monotonic wheezing heard louder at the level of the larynx indicates an upper airway obstruction, regardless of the etiology. Stridor is heard prominently when the airflow is maximal or the airway lumen decreases. Inspiratory stridor strongly suggests palatal, tracheal, laryngeal, or epiglottic obstruction, and may indicate a medical emergency. Expiratory stridor suggests an obstruction in the lower airways or in a bronchus, as caused by a foreign body.

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Turning to Spirometry for Clarification

Spirometry can be helpful in further delineating the site and cause of wheezing. A low forced expiratory volume in one second (FEV1), with significant reversibility after administration of a bronchodilator, indicates asthma. In patients with normal spirometry findings, asthma can be diagnosed by bronchoprovocation with methacholine or histamine. The configuration and changes of the spirometric flow-volume loop (see examples below) help in diagnosing other conditions such as upper airway obstruction.

A flow-volume loop can also help to differentiate between variable intrathoracic and extrathoracic obstruction. However, it is important to remember that spirometric abnormalities are not seen until obstruction is advanced (see table below).

Spirometric Diagnosis of Obstruction: Hints and Caveats FEV1 is a poor indicator of large airway obstruction In general, the airway abnormality has to decrease the tracheal lumen to less than 8mm before the flow-volume loop (FVL) is abnormal. In patients with severe COPD, even a significant tracheal stenosis may not be apparent on FVL. FVL abnormality indicates the functional rather than the anatomic severity of the obstruction Baseline resting stridor usually indicates that the airway lumen is less than 5mm.

There are three main patterns of obstruction identified by the flow-volume loop: variable intrathoracic, variable extrathoracic, and fixed (see table below). A variable lesion is one subject to changes in airway pressures, which differ by location. Airway diameter and flows are influenced by surrounding atmospheric pressures in the extrathoracic airway and by pleural pressures in the intrathoracic airway.

Causes of Variable and Fixed Upper Airway Obstruction
Variable Extrathoracic Tracheomalacia Vocal cord paralysis Vocal cord dysfunction Vocal cord polyps	Variable Intrathoracic Tracheomalacia of intrathoracic airway Tumors Mediastinal adenopathy	Fixed Tracheal stenosis Subglottic (as caused by intubation, Wegener's granulomatosis) Tracheal (as caused by intubation) Tracheal tumors Foreign body

Variable extrathoracic obstruction. During inspiration, the pressure around the extrathoracic airway is atmospheric, and the transmural pressure favors narrowing. This is not clinically important in normal individuals. However, in the presence of a nonrigid extrathoracic obstruction, such as bilateral vocal cord paralysis, there is a decrease in airway pressure distal to the obstruction, which causes further narrowing and obstruction of the airway (see illustration below). The flow-volume loop will show a flattening of the inspiratory component. Other examples of variable extrathoracic obstruction are tracheomalacia of the extrathoracic trachea and vocal cord dysfunction.

Variable extrathoracic obstruction. During forced expiration, intratracheal pressure (Ptr) becomes greater than atmospheric pressure (Patm), and airway size remains near normal (left). During inspiration, Patm is higher than Ptr, worsening the obstruction and decreasing inspiratory airflow (center). The flow-volume loop shows flattening of the inspiratory limb.

Variable intrathoracic obstruction. During forced expiration, the pleural pressure becomes positive relative to the airway pressure, which favors narrowing of the intrathoracic airway. In a normal person this effect does not have clinical significance, but in the presence of an intrathoracic disorder (such as intrathoracic tracheomalacia) it may worsen the obstruction (see illustration below). In the flow-volume loop it is seen as a flattening of the expiratory component.

Variable intrathoracic obstruction. During forced expiration, the intrapleural pressure (Ppl) becomes greater than the intratracheal pressure (Ptr), worsening the obstruction and decreasing expiratory flow (left). During inspiration, Ptr is greater than Ppl, improving the airway diameter (center). The flow-volume loop shows flattening of the expiratory limb.

Fixed upper airway obstruction. When the airway obstruction is rigid, as in tracheal stenosis or intraluminal tumors (benign or malignant), the flow will be limited during both inspiration and expiration, flattening both components of the flow-volume loop (see example below).

Flow-volume loop of a fixed airway obstruction. Inspiratory and expiratory flow rates are decreased, leading to flattening of both limbs.

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Roles of Diagnostic Imaging and Endoscopy

Plain chest radiographs are helpful in the workup of a patient with wheezing. Consolidation in a patient with eosinophilia suggests one of the eosinophilic syndromes. Infiltrates in the superior segment of the lower lobes or posterior segment of the upper lobes indicate aspiration pneumonitis. The combination of an enlarged cardiac silhouette, cephalization of blood flow, and pleural effusions points to congestive heart failure as the cause of wheezing.

Atelectasis of a segment of one or more lobes suggests volume loss due to the presence of an endobronchial tumor or a foreign body. Plain x-ray films may show hilar or mediastinal lymphadenopathy, contributing to airway compression and volume loss.

Plain neck films may show narrowing of the subglottic space on posteroanterior views, known as the steeple sign, which is the classic sign for croup. The lateral neck film is more helpful for diagnosing epiglottitis, showing a swollen epiglottis, hypopharyngeal dilatation, or both. However, the overall sensitivity of neck films for diagnosis of either croup or epiglottitis is only 38% to 54%.

Computed tomography (CT) scanning of the chest and neck is helpful when evaluating airway compression due to lymph nodes, tumors, and other lesions. The disadvantage of conventional CT, however, is the inability to image the trachea along its long axis. Spiral CT with multiplanar and three-dimensional reconstructions allows better assessment of the extent of disease. Some studies have shown similar sensitivity and specificity when spiral CT was compared with bronchoscopy in the evaluation of upper airway structural abnormalities, such as intraluminal tumors (benign and malignant) or tracheal stenosis.

Magnetic resonance imaging can also be used and offers several advantages, including resolution without contrast injection, good mediastinal evaluation, and estimation of the length and degree of tracheal obstruction.

In recent years, rhinolaryngoscopy and flexible fiberoptic bronchoscopy performed under local anesthesia have dramatically improved diagnostic accuracy for a large number of conditions that can present as "wheezing" accompanied by other respiratory symptoms. The inspection of the upper and lower airways might be the final test to confirm diagnoses such as vocal cord paralysis, vocal cord dysfunction, laryngeal polyps and granulomas, tracheal stenosis, and endotracheal or endobronchial lesions.

Following are two case examples that will illustrate the diagnosis and treatment of asthma mimics.

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Case Example: Vocal Cord Dysfunction

A 32-year-old obese woman has been receiving treatment for asthma in a clinic for five years. Her asthma has been difficult to control, with recurrent episodes of exacerbation in spite of appropriate therapy. During the previous year she had made 10 visits to the emergency room, and she is currently taking maximum doses of inhaled steroids, long-acting beta-agonists, oral prednisone 20 mg/day, leukotriene inhibitors, and inhaled albuterol as needed. Her spirometry results in the clinic were normal, but a methacholine challenge test was positive for reactive airway disease. During the last emergency room visit, the physician found the patient in moderate to severe respiratory distress, anxious, and with bilateral diffuse wheezing, which was prominent over the neck. The patient was hypoxemic, but there was no increased P(A-a)O2 gradient. Very astutely, the physician provided care for the "asthma attack" but at the same time requested a laryngoscopic evaluation, which confirmed the diagnosis of vocal cord dysfunction (VCD) (see endoscopic image below).

Vocal cord dysfunction. Direct laryngoscopy shows the anterior two thirds of the vocal cords approximating during inspiration (left arrow), leaving a small diamond-shaped "chink" opening posteriorly (right arrow). This finding confirms the diagnosis of VCD.

General features. In VCD, the anterior two-thirds of the vocal cord close, leaving only a 4- to 5-mm diamond-shaped posterior "chink" for airflow. The airway closure usually occurs during inspiration but can be seen during expiration as well. In the past, this disorder has been called factitious asthma, hysterical stridor, Munchausen's stridor, psychogenic upper airway obstruction, and fake asthma. Patients may present with wheezing, stridor, or both. Vocal cord dysfunction has been described in patients as young as 3 and as old as 82 years old, but most commonly it is seen in the second to fourth decade, in overweight patients, and among health professionals (around 25% of cases). A number of these patients have a prior diagnosis of asthma, generally considered refractory to standard therapy. (It is important to remember that VCD and asthma are not mutually exclusive.) About half take oral steroids.

A study from the National Jewish Center in Denver identified 95 patients diagnosed with VCD by laryngoscopic evaluation. Of these, 53 had concomitant asthma. The patients in the group without asthma were receiving daily prednisone at an average daily dose of 29 mg and had made 9.7 emergency room visits and were admitted to the hospital 5.9 times in the year prior to presentation. About a third of these patients had been intubated.

Acute attacks can be accompanied by hoarseness and dysphonia. The patient may point to the throat as the cause of respiratory distress. Attacks can be precipitated by upper respiratory infections and irritants such as dust and smoke. When the problem is purely VCD, the patient rarely is awakened by it at night. The physical exam may be helpful but is unreliable in differentiating VCD from asthma.

Diagnostic keys. A high index of suspicion in a patient refractory to asthma treatment or presenting with upper airway obstruction is crucial to making the diagnosis of VCD. Stressful situations may increase the degree of paradoxical vocal cord motion. Between episodes, spirometry results and flow volume loop curves are normal. During the acute attack, hypoxemia may be present, but usually without an increased P(A-a)O2 (alveolar-arterial oxygen tension) gradient. The spirometry readings might show a flattening of the inspiratory limb of the flow-volume loop. Laryngoscopy during the acute attack is the gold standard for establishing the diagnosis. Adduction of the anterior two thirds of the cords, causing a posterior diamond-shaped opening to appear, is usually seen during inspiration but may occur during expiration or both.

Therapy. In VCD, it is essential to withdraw unnecessary treatment, such as steroids. Speech therapy and psychotherapy have been used with some success. During the acute attack, offering reassurance to the patient is important. Heliox (80:20 helium-oxygen mixture, a low-density gas) increases airflow across the narrowed airway and may avert the need for invasive treatment. Overall, the results of the long-term therapies seem to be disappointing.

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Case Example: Airway Obstruction

A 33-year-old nonsmoking man presented to the emergency department with shortness of breath, cough, and wheezing of 10 days' duration. One year before this visit, the patient had a lengthy hospitalization after a motor vehicle accident and required intubation and prolonged mechanical ventilation. He also had a history of asthma during childhood. Because of his symptoms and the history of asthma, he was given several bronchodilator treatments, but his response was minimal. The patient was admitted to the intensive care unit, where he was found to be tachycardic and in moderate respiratory distress. The clinician noted that his wheezing was more intense on auscultation of the neck. A tracheostomy scar was found. Based on the finding of clear lungs with stridor, portable spirometry was performed (see figure below)
.

Fixed airway obstruction. This flow-volume loop shows flattening of both inspiratory and expiratory limbs, consistent with the diagnosis of tracheal stenosis.

A laryngoscopy showed subglottic tracheal stenosis at the site of previous tracheostomy, which confirmed the diagnosis of upper airway obstruction secondary to tracheal stenosis.

General features. Upper airway obstruction can be divided into structural and functional obstruction (see table below). Anatomic obstructions are caused by lesions or diseases that narrow the airway lumen, such as tracheal stenosis. Functional obstructions, on the other hand, might not have an obvious, visible lesion but can cause dynamic collapse of the airway during the respiratory cycle (as in obstructive sleep apnea).

Causes of Upper Airway Obstruction Anatomic Soft tissue infection Ludwig's angina Retropharyngeal abcess Laryngeal or tracheal tumors Intraluminal obstruction Laryngeal stenosis (as occurs with intubation) Tracheal stenosis (as occurs after tracheostomy) Foreign body (especially in children) Infiltrating diseases Sarcoidosis Amyloidosis Wegener's granulomatosis Web, stricture, or ring (especially in children) Mucosal edema associated with burns or reflux Laryngotracheobronchitis or epiglottitis Extrinsic compression Goiter Innominate artery aneurysm Mediastinal masses Esophageal foreign body Esophageal achalasia Mucous ball from transtracheal catheters   Functional Vocal cord paralysis Unilateral (as in laryngeal nerve damage) Bilateral (as in post thyroidectomy) Vocal cord dysfunction Laryngospasm Obstructive sleep apnea Tracheo- and bronchomalacia Upper airway laxity (as in sleep apnea)

Worsening symptoms occur when demand for minute ventilation increases through a narrow opening, as during exercise, or when the narrowed lumen is further compromised due to an upper respiratory infection. In the case described above, the previous intubation, tracheostomy, or both probably caused the tracheal stenosis, since endotracheal intubation can lead to damage of the glottis with such consequences as vocal cord paralysis. Factors that have been found to increase the risk of laryngeal injury include tracheostomy, severe laryngeal trauma during extubation, large endotracheal tube caliber, oral intubation, severe respiratory failure, diabetes, and female gender.

The incidence of all types of injury to the larynx after intubation ranges from 63% to 94%. Significant airway stenosis occurs in 6% to 12% of cases. Because of the risk of intubation-associated airway injury, tracheostomy is generally recommended after two weeks of endotracheal intubation. The incidence of tracheal stenosis secondary to intubation was as high as 20% in the past but has waned since the introduction of low-pressure, high-volume cuffs. The incidence of tracheal stenosis following tracheotomy varies, and it can occur at the site of the stoma, cuff, or tip. Severe stenosis requiring surgical intervention occurs in less than 8% of patients.

Diagnostic keys. A history of intubation with or without tracheostomy, progressive shortness of breath, stridor, and a normal lung exam should prompt the physician to evaluate for the presence of tracheal stenosis.

Treatment. Emergency treatment of upper airway obstruction depends on the etiology of the obstruction. Racemic epinephrine can be used to treat croup and may also be used empirically in the treatment of laryngeal edema. Heliox has been shown to decrease the turbulent airflow generated at the area of obstruction and the flow-resistive work. Heliox has been used for postextubation stridor, tracheal stenosis, intrinsic compression, VCD, status asthmaticus, and angioedema. It is only a temporizing solution until the primary event is resolved or more definitive therapy is instituted.

For soft tissue infection such as Ludwig's angina or retropharyngeal abscess, surgical drainage and intravenous antibiotics are indicated. The incidence of epiglottitis has decreased in the last few years with the use of the vaccine for type B Haemophilus influenzae. An artificial airway and intravenous antibiotics have decreased mortality from 6.1% to less than 1.0%. Adults who aspirate a foreign body sometimes relate a history of choking, but as previously noted, one in three may not recall any such episode. Endoscopic evaluation is needed in most aspiration cases.

Unilateral vocal cord paralysis usually causes hoarseness but is not accompanied by significant respiratory distress. However, it can lead to difficulties in swallowing and recurrent aspiration. The paralyzed vocal cord may be augmented by injecting a Teflon suspension or be addressed via laryngoplasty with insertion of material that moves the vocal cord medially.

Bilateral vocal cord paralysis (after thyroidectomy, for example) may be missed because of near-normal phonation. The patient might remain relatively asymptomatic at rest but may be symptomatic during exercise or an upper respiratory infection. Tracheostomy is generally required to relieve the obstruction.

Patients with suspected obstructive sleep apnea should undergo a diagnostic and a titration study to determine the amount of positive airway pressure needed to relieve the obstruction. Surgery of the upper airway may benefit a select group of patients.

In patients with evidence of tracheal stenosis, several therapeutic options are available including balloon dilatation, laser therapy, stent placement, and resection. Laser therapy can be palliative for patients with malignant tracheobronchial lesions. Lasers also can excise weblike tracheal stenosis and treat benign granulomatous lesions obstructing the airway. Bronchoscopic dilatation is another option in subglottic and tracheal stenosis, using either a rigid bronchoscope or Jackson dilators. This is usually a temporizing measure, since most symptoms recur. Resecting the stenotic segment and reanastomosing the remaining segments is also possible; the success rate is about 87% when the procedure is performed by experienced hands.

Stent placement can also be used to treat subglottic and tracheal obstruction and is most beneficial in treating lower tracheobronchial benign lesions. In malignant lesions, the tumor usually recurs and reoccludes the opened airway. For distal obstructions, other invasive techniques are used for palliation. Some of the methods in addition to stents are radiation (external or local brachytherapy), laser therapy, cryotherapy, and bronchoscopic debulking of the lesion with forceps.

Suggested Reading Aboussouan LS and Stoller JK: Diagnosis and management of upper airway obstruction. Clin Chest Med 15:35, 1994. Christopher KL, et al.: Vocal-cord dysfunction presenting as asthma. N Engl J Med 308:1566, 1983. Guntupalli K, et al.: Usefulness of flow volume loops in emergency center and ICU settings. Chest 111:481, 1997. Holden DA and Mehta AC: Evaluation of wheezing in the nonasthmatic patient. Cleve Clin J Med 90:345, 1990. Hyatt RE and Black LF: The flow-volume curve. Am Rev Respir Dis 107:191, 1973. Kryger M, et al.: Diagnosis of obstruction of the upper and central airway. Am J Med 61:87, 1976. Miller RD and Hyatt R: Evaluation of obstructing lesions of the trachea and larynx by flow-volume loops. Am Rev Respir Dis 108:475, 1973. Miller RD and Hyatt RE: Obstructing lesions of the larynx and trachea: Clinical and physiologic characteristics. Mayo Clin Proc 44:145, 1969. Newman KB, et al.: Clinical features of vocal cord dysfunction. Am J Respir Crit Care Med 152:1382, 1995. Whyte RI, et al.: Helical computed tomography for the evaluation of tracheal stenosis. Ann Thorac Surg 60:27, 1995.

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