augment respiratory drive, and patients with hyperthyroidism and pregnant women commonly report dyspnea. Dyspnea during pregnancy often starts before the abdomen is noticeably distended, indicating that diaphragmatic elevation from the enlarging uterus is not the primary explanation for the dyspnea.

Dyspnea may also be due to or exacerbated by several factors, such as deconditioning and obesity, that do not readily fall into the above-mentioned clinical categories. An individual who is deconditioned, often because of a sedentary lifestyle and little exercise, is less able than the well-conditioned individual to augment cardiac output for delivering oxygen to exercising muscles. Though significant obesity is often accompanied by deconditioning, it may also be associated with increased ventilatory requirements as well as increased work of breathing, leading to the exertional dyspnea commonly experienced by significantly obese individuals even in the absence of underlying cardiopulmonary disease. Finally, anxiety may also contribute to or cause a sensation of dyspnea, which may be disproportionately noticed during rest rather than during exercise. Because the sensation of dyspnea is so subjective, any awareness of one’s breathing may start a self-perpetuating problem. The patient breathes faster, becomes more aware of breathing, and finally has a sensation of shortness of breath. At the extreme, a person can hyperventilate and lower arterial PCO2 sufficiently to cause additional symptoms of lightheadedness and tingling, particularly of the fingers and around the mouth. Of course, patients who seem anxious can also have lung disease, just as patients with lung or heart disease can have dyspnea with a functional cause unrelated to their underlying disease process.

Cough

Cough is a symptom everyone has experienced at some point. It is a physiologic mechanism for clearing and protecting the airway and does not necessarily imply disease. Normally, cough is protective against food or other foreign material entering the airway. It also is responsible for helping clear secretions produced within the tracheobronchial tree. Generally, mucociliary clearance is adequate to propel secretions upward through the trachea and into the larynx so that the secretions can be removed from the airway and swallowed. However, if the mucociliary clearance mechanism is temporarily damaged or not functioning well, or if the mechanism is overwhelmed by excessive production of secretions, coughing becomes an important additional mechanism for clearing the tracheobronchial tree.

Cough usually is initiated by stimulation of receptors (called irritant receptors) at several locations. Irritant receptor nerve endings are found primarily in the larynx, trachea, and major bronchi, particularly at points of bifurcation. However, sensory receptors are also located in other parts of the upper airway as well as on the pleura, the diaphragm, and even the pericardium. Irritation of these nerve endings initiates an impulse that travels via afferent nerves (primarily the vagus, but also trigeminal, glossopharyngeal, and phrenic) to a poorly defined cough center in the medulla. The efferent signal is carried in the recurrent laryngeal nerve (a branch of the vagus), which controls closure of the glottis, and in phrenic and spinal nerves, which effect contraction of the diaphragm and the expiratory muscles of the chest and abdominal walls. The initial part of the cough sequence is a deep inspiration to a high lung volume, followed by closure of the glottis, contraction of the expiratory muscles, and opening of the glottis. When the glottis suddenly opens, contraction of the expiratory muscles and relaxation of the diaphragm produce an explosive rush of air at high velocity, which transports airway secretions or foreign material out of the tracheobronchial tree.

Irritant receptors triggering cough are located primarily in larger airways.

The major causes of cough are listed in Table 2.2. Cough commonly results from an airway irritant, regardless of whether the person has respiratory system disease. The most common inhaled irritant is

TABLE 2.2

Differential Diagnosis of Cough

Airway Irritants

Inhaled smoke, dusts, and fumes

Aspiration

Gastric contents

Oral secretions

Foreign bodies

Postnasal drip (upper airway cough syndrome)

Airway Disease

Upper respiratory tract infection

Postinfectious cough

Acute or chronic bronchitis

Eosinophilic bronchitis

Bronchiectasis

Neoplasm

External compression by node or mass lesion

Reactive airway disease (asthma)

Parenchymal Disease

Pneumonia and other lower respiratory tract infections (e.g., tuberculosis)

Lung abscess

Interstitial lung disease

Congestive Heart Failure

Miscellaneous

Drug-induced (angiotensin-converting enzyme inhibitors)

Cough hypersensitivity syndrome

Cough caused by respiratory system disease derives mainly but not exclusively from disorders affecting the airway. Upper airway infections, most commonly caused by viruses or certain bacteria (especially Mycoplasma, Chlamydophila, and Bordetella pertussis), also affect parts of the tracheobronchial tree, and the airway inflammation results in a bothersome cough that sometimes lasts from weeks to months. Bacterial infections of the lung, either acute (pneumonia and acute bronchitis) or chronic (bronchiectasis, chronic bronchitis, and lung abscess), generally have an airway component and an impressive amount of associated coughing. Space-occupying lesions in the tracheobronchial tree

(tumors, foreign bodies, and granulomas) and external lesions compressing the airway (mediastinal masses, lymph nodes, and other tumors) commonly manifest as cough secondary to airway irritation. Hyperirritable airways with airway constriction, such as in asthma, are frequently associated with cough, even when a specific inhaled irritant is not identified. The more readily recognized manifestations of asthma (wheezing and dyspnea) may not be apparent, and cough may be the sole presenting symptom, in which case the term cough variant asthma is applied. An entity of unknown etiology called nonasthmatic eosinophilic bronchitis, characterized by eosinophilic inflammation of the airway in the absence of asthma, has also been identified as a cause of chronic cough.

Patients with diffuse parenchymal (interstitial) lung disease may have cough, probably owing more to secondary airway or pleural involvement, because very few irritant receptors are present in the lung parenchyma. In heart failure, cough may be related to the same unclear mechanism operative in patients with diffuse parenchymal lung disease, or it may be secondary to bronchial edema.

A variety of miscellaneous causes of cough, such as irritation of the tympanic membrane by wax or a hair or stimulation of one of the afferent nerves by osteophytes or neural tumors, have been identified but are not discussed in further detail here. With the widespread use of angiotensin-converting enzyme (ACE) inhibitors (e.g., enalapril and lisinopril) for treatment of hypertension and heart failure, cough has been recognized as a relatively common side effect of these agents. Because ACE breaks down bradykinin and other inflammatory peptides, accumulation of bradykinin or other peptides in patients taking these inhibitors may be responsible by stimulating receptors capable of initiating cough. Of note, cough is a far less common side effect of angiotensin II receptor antagonists such as losartan, although it may occur. Coughing may be a nervous habit that can be especially prominent when the patient is anxious, although the physician must not neglect the possibility of an organic cause.

A relatively recently recognized entity of cough hypersensitivity syndrome describes an increased sensitivity of airway sensory receptors to irritant stimuli. It can manifest clinically as a chronic, unexplained cough or as a generalized increased sensitivity to environmental or other stimuli that can provoke coughing.

The symptom of cough is generally characterized by whether it is productive or nonproductive of sputum. Virtually any cause of cough may be productive at times of small amounts of clear or mucoid sputum. However, thick yellow or green sputum indicates the presence of numerous leukocytes in the sputum, either neutrophils or eosinophils. Neutrophils may be present with just an inflammatory process of the airways or parenchyma, but they also frequently reflect the presence of a bacterial infection. Specific examples include bacterial bronchitis, bronchiectasis, lung abscess, and pneumonia. Eosinophils, which can be seen after special preparation of the sputum, often occur with bronchial asthma, whether or not an allergic component plays a role, and in the much less common entity of nonasthmatic eosinophilic bronchitis.

Yellow or green sputum reflects the presence of numerous leukocytes, either neutrophils or eosinophils.

In clinical practice, cough is often divided into three major temporal categories: acute, subacute, or chronic, depending on the duration of the symptom. Acute cough, defined by a duration of less than 3 weeks, is most commonly due to an acute viral infection of the respiratory tract, such as the common cold. Subacute cough is defined by a duration of 3 to 8 weeks, and chronic cough lasts 8 or more weeks. Chronic bronchitis is a particularly frequent cause of cough in smokers, whereas common causes of either subacute or chronic cough in nonsmokers are postnasal drip (also called upper airway cough syndrome), gastroesophageal reflux, and asthma. An important subacute cough is postinfectious cough that lasts for more than 3 weeks following an upper respiratory tract infection. It often is due to persistent airway

inflammation, postnasal drip, or bronchial hyperresponsiveness (as seen with asthma). In all cases,

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