DYSPNEA
Thursday, March 5, 2009
Dyspnea is a common symptom. It is analogous to pain in that sensory input from multiple sites in the respiratory system 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 airflow limitation or exercise tolerance and the severity of dyspnea.
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, hypoxemia a weak one. 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. Stimulation of irritant receptors in the airways intensifies dyspnea, while stimulation of pulmonary stretch receptors decreases it.
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. The clinician can assess dyspnea and response to treatment with a ten-point 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?” 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. A complete allergic, occupational, and smoking history is essential.
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 suggest asthma, gastroesophageal reflux disease (GERD), left ventricular dysfunction, or obstructive sleep apnea. Rapid onset of severe dyspnea when supine suggests phrenic nerve impairment and diaphragmatic paralysis. Platypnea (dyspnea that worsens in the upright position) is a rare complaint associated with arteriovenous malformations at the lung bases, resulting in increased shunting and hypoxemia in the upright position (orthodeoxia).
Chronic dyspnea is invariably 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.
Dyspnea is increasingly being recognized as a major issue in the care of dying patients, and clinicians typically undertreat this symptom.
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. 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 4–6 hours. Pulmonary rehabilitation can improve respiratory function and train patients in energy conservation and breathing techniques that help moderate their sense of respiratory effort. Opioids reduce respiratory drive and blunt dyspnea. They can be titrated safely even in patients with advanced lung disease. 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.
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, hypoxemia a weak one. 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. Stimulation of irritant receptors in the airways intensifies dyspnea, while stimulation of pulmonary stretch receptors decreases it.
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. The clinician can assess dyspnea and response to treatment with a ten-point 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?” 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. A complete allergic, occupational, and smoking history is essential.
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 suggest asthma, gastroesophageal reflux disease (GERD), left ventricular dysfunction, or obstructive sleep apnea. Rapid onset of severe dyspnea when supine suggests phrenic nerve impairment and diaphragmatic paralysis. Platypnea (dyspnea that worsens in the upright position) is a rare complaint associated with arteriovenous malformations at the lung bases, resulting in increased shunting and hypoxemia in the upright position (orthodeoxia).
Chronic dyspnea is invariably 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.
Dyspnea is increasingly being recognized as a major issue in the care of dying patients, and clinicians typically undertreat this symptom.
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. 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 4–6 hours. Pulmonary rehabilitation can improve respiratory function and train patients in energy conservation and breathing techniques that help moderate their sense of respiratory effort. Opioids reduce respiratory drive and blunt dyspnea. They can be titrated safely even in patients with advanced lung disease. 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.
2 comments:
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