PULMONOLOGY, DYSPNEA

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]