DYSPNEA

Dyspnea is a common symptom. It is analogous to hunger or nausea in that sensory input from multiple sites is integrated in the cerebral cortex. In general, dyspnea increases with the level of functional impairment as measured by spirometry. However, there is only a weak correlation between the severity of dyspnea and quantitative measures of airflow limitation or exercise tolerance.
Several pathophysiologic processes contribute to dyspnea. The most important is the increased respiratory effort that accompanies many different diseases: airflow obstruction (asthma; chronic obstructive pulmonary disease [COPD]), changes in pulmonary compliance (interstitial fibrosis, congestive heart failure) or chest wall compliance (obesity, pleural disease), intrinsic respiratory muscle weakness (inanition, neuromuscular disease, chronic respiratory failure), or the weakness conveyed by the mechanical disadvantage of hyperinflation (asthma or emphysema). Dyspnea is magnified by increased respiratory drive. Acute hypercapnia is therefore a potent stimulus to dyspnea, while hypoxemia is usually a weak one. Stimulation of irritant receptors in the airways intensifies dyspnea, while stimulation of pulmonary stretch receptors decreases it. In mechanically ventilated patients, failure to provide adequate inspiratory flow rates to patients with heightened respiratory drive commonly results in dyspnea that may present as agitation.
Clinical Findings
The history should focus on onset and timing of symptoms, the patient's position at onset of symptoms, the relationship of symptoms to activity, and any factors that may improve or exacerbate symptoms. Complete allergic, occupational, and smoking histories are essential. Exertional dyspnea should be quantified, but the absolute level of exertion that precipitates dyspnea is less important than acute changes in the threshold level of activity. The clinician can assess dyspnea and response to treatment with a numeric rating scale by asking the patient, "On a scale of zero to ten, with zero being no shortness of breath and ten being the worst shortness of breath you can imagine, how short of breath are you?"
Acute dyspnea has a short list of causes, most of which are readily identified: asthma, pulmonary infection, pulmonary edema, pneumothorax, pulmonary embolus, metabolic acidosis, or acute respiratory distress syndrome (ARDS). Panic attacks may present as a respiratory complaint. Orthopnea (dyspnea on recumbency) and nocturnal dyspnea suggests asthma, gastroesophageal reflux disease, left ventricular dysfunction, or obstructive sleep apnea. Rapid onset of severe dyspnea when supine suggests phrenic nerve impairment leading to diaphragmatic weakness or paralysis. Platypnea (dyspnea that worsens in the upright position) is a rare complaint associated with arteriovenous malformations at the lung bases or with hepatopulmonary syndrome, resulting in increased shunting and hypoxemia in the upright position (orthodeoxia).
Chronic dyspnea is typically progressive. Symptoms often first appear during exertion; patients learn to limit their activity to accommodate their diminished pulmonary reserve until dyspnea occurs with minimal activity or at rest. Episodic dyspnea suggests congestive heart failure, asthma, acute or chronic bronchitis, or recurrent pulmonary emboli. Constant dyspnea is most commonly due to COPD but may indicate interstitial lung disease (eg, pulmonary fibrosis), pulmonary vascular disease, or fixed airflow obstruction from severe asthma.
Evaluation should include a complete blood count, renal function tests, chest radiograph, spirometry, and noninvasive oximetry. Patients over 40 years of age or with a family history of early coronary disease should have an electrocardiogram. Arterial blood gases, measurement of lung volumes, ventilation-perfusion (
/
) scanning, echocardiography, and cardiopulmonary exercise testing are reserved for cases that elude diagnosis on initial evaluation.
Treatment
In patients with advanced lung disease, the responsible condition may be easily identified but treatment only partially effective. Oxygen improves survival in those who are hypoxemic and can improve the exercise tolerance of all patients. Its effect on dyspnea is variable. Opioids reduce respiratory drive and blunt dyspnea. They can be titrated safely even in patients with advanced lung disease. Anxiety can play an important role in the distress caused by dyspnea and may be relieved by judicious use of benzodiazepines such as lorazepam, 0.5–1 mg orally every 6–8 hours. Pulmonary rehabilitation can improve respiratory function and train patients in energy conservation and breathing techniques that help moderate their sense of respiratory effort. Finally, fresh air or a fan may offer additional relief. Smokers with progressive exertional dyspnea should know that they can limit future loss of function through smoking cessation.
Dyspnea is increasingly being recognized as a major issue in the care of dying patients, and clinicians typically under treat this symptom. See Palliative Care & Pain Management.

Dyspnea. Mechanisms, assessment, and management: a consensus statement. American Thoracic Society. Am J Respir Crit Care Med. 1999 Jan;159(1):321–40. [PMID: 9872857]

Karnani NG et al. Evaluation of chronic dyspnea. Am Fam Physician. 2005 Apr 15;71(8):1529–37. [PMID: 15864893]

Luce JM et al. Management of dyspnea in patients with far-advanced lung disease: "once I lose it, it's kind of hard to catch it. . ." JAMA. 2001 Mar 14;285(10):1331–7. [PMID: 11255389]




COUGH
Cough is an important physiologic mechanism that defends against respiratory pathogens and helps clear the tracheobronchial tree of mucus, foreign particles, and noxious aerosols. Excessive cough is one of the most common symptoms for which patients seek medical care and may represent up to one-third of a pulmonologist's outpatient practice referrals. Persistent severe cough, seen in interstitial lung disease or bronchiectasis, may impair respiration as well as disrupt sleep and social functioning. Bronchospasm (brought on by repetitive forced exhalation), syncope, rib fractures, and urinary incontinence are all potential complications. A reduced or absent cough, seen in some postoperative patients or those with neuromuscular disease, will reduce clearance of secretions and may impair oxygenation.
Cough may be voluntary or involuntary. Involuntary cough is stimulated by vagal afferent receptors in the trachea, especially at the carina, and the larynx but also from others throughout the head and neck. Stimulation of cough receptors may be mechanical, as in cases of aspiration, or irritative.
Clinical Findings
It is important to distinguish acute (< 3 weeks) from subacute (3–8 weeks) and chronic (> 8 weeks) cough. Acute cough most commonly follows viral or bacterial upper respiratory tract infection. Within 2 days after onset of the common cold, 85% of untreated patients cough; 25% are still coughing 14 days later; in a few, cough will persist for 6–8 weeks. Many patients with persistent cough following upper respiratory tract infection have underlying asthma. Other causes of acute cough include aspiration, pneumonia, pulmonary embolism, and pulmonary edema.
The most common cause of chronic cough is a low-grade chronic bronchitis secondary to exposure to tobacco smoke, though smokers do not commonly seek medical attention for this problem. Over 90% of nonsmokers presenting for evaluation of chronic cough suffer from postnasal drip, gastroesophageal reflux disease, or asthma (even without other symptoms). Angiotensin-converting enzyme (ACE) inhibitors have become another common cause. In primary care settings, single causes predominate.
The character and timing of chronic cough and the presence or absence of sputum production do not permit an etiologic diagnosis and should not be used as the sole basis for empiric therapy. The history and physical examination should attempt to identify anatomic locations of the afferent limb of the cough reflex in light of the common causes listed above. A nasal discharge, frequent need to clear the throat, and mucoid or mucopurulent secretions in the posterior pharynx suggest an upper airway cough syndrome. Sinus imaging may be diagnostic of acute or chronic sinusitis. Wheezing on chest auscultation or airflow obstruction on pulmonary function tests suggests asthma. In cough-variant asthma, methacholine bronchoprovocation testing may be positive in the absence of clinical findings of asthma. Gastroesophageal reflux disease is an important cause of chronic cough but is associated with the fewest clinical clues; cough, even in the absence of heartburn, may be the only symptom. Barium swallow is specific but insensitive, and esophageal pH monitoring may be necessary for diagnosis. Chest imaging is best reserved for evaluation of cough in smokers; in patients with hemoptysis or constitutional symptoms, such as fever and weight loss; and in persons with chronic cough that does not respond to initial therapy.
Treatment
See Related Guideline from CURRENT Practice Guidelines in Primary Care 2007
The first step is to eliminate irritant exposures such as tobacco smoke (primary or secondary) and occupational agents and to discontinue medications such as ACE inhibitors or
-blockers, including eyedrops. Cough due to ACE inhibitors should subside within 1–4 days after discontinuing the medication, though it may take several weeks. Upper airway cough syndrome due to allergic rhinitis that does not respond to antihistamines should be treated with intranasal corticosteroids. Chronic sinusitis may require prolonged antibiotics directed against Haemophilus influenzae. Cough caused by asthma that does not respond after 2 weeks of bronchodilators and corticosteroids suggests another contributing condition. Cough due to gastroesophageal reflux disease is difficult to treat and may require proton pump inhibitors, since H2-blockers may be inadequate. Patients whose cough began after an upper respiratory tract infection usually respond to treatment with an antihistamine-decongestant combination or treatment for asthma.

Chang AB et al. Gastro-oesophageal reflux treatment for prolonged non-specific cough in children and adults. Cochrane Database Syst Rev. 2005 Apr 18;(2):CD004823. [PMID: 15846735]

Diagnosis and management of cough: ACCP evidence-based clinical practice guidelines. Chest. 2006 Jan;129(1 Suppl):1S–292S. [PMID: [PMID: 16428686 through 16428721]

Hewlett EL et al. Clinical practice. Pertussis—not just for kids. N Engl J Med. 2005 Mar 24;352(12):1215–22. [PMID: 15788498]

Morice AH et al; ERS Task Force. The diagnosis and management of chronic cough. Eur Respir J. 2004 Sep;24(3):481–92. [PMID: 15358710]