Quality of Dyspnea Directs Diagnosis, Management



KEYSTONE, COLO. – Understanding the quality of a patient’s dyspnea provides insights into the underlying physiologic mechanism and can guide management, according to Dr. James T. Good Jr., a pulmonologist at National Jewish Health in Denver.

Complaints that may represent dyspnea can be as vague as fatigue, lack of energy, or simply getting old, but most commonly are a sensation of air hunger, of work or effort to breathe, or of chest tightness. All three sensations are the result of a mismatch or neuromechanical dissociation between ongoing motor signals to the respiratory muscles and incoming afferent information from the lungs, chest wall, and upper airways, Dr. Good said at a meeting on allergy and respiratory diseases.

Dr. James T. Good Jr.

For the patient who describes air hunger, the sensation can be equated to being held underwater and is often so distressing that patients say they would prefer pain to air hunger. The sensation is mediated primarily through central and peripheral chemoreceptors and stimulated by hypercapnia or hypoxia in the presence of decreased arterial carbon dioxide (CO2) partial pressure and oxygen partial pressure, Dr. Good said.

In the patient who describes work or effort when breathing, the sensation is stimulated by respiratory motor muscle contraction and muscle fatigue and is mediated through a combination of central motor discharge, chest wall receptors, and metaboreceptors located within skeletal muscle, he said at the meeting, which was sponsored by National Jewish Health.

In patients with chest tightness, the sensation is stimulated by bronchoconstriction and tends to be mediated primary through rapidly adapting stretch receptors (RARs) and C-fiber receptors in the pulmonary and respiratory tract. Chest tightness can occur with other dyspneic sensations but is fairly specific to asthma and chronic obstructive pulmonary disease (COPD).

The first question to ask patients who present with complaints of an uncomfortable sensation associated with breathing is whether it occurs at rest or with exertion, Dr. Good suggested. Dyspnea at rest implies an acute illness or moderate to severe cardiopulmonary disease. It also is very common in patients with anxiety, with or without underlying disease, and in patients with alterations in the respiratory drive. Dyspnea with exertion is most common in patients with cardiac dysfunction, pulmonary diseases, metabolic disorders, deconditioning, obesity, and anemia.

The next important question to ask is whether the patient with dyspnea has normal oxygen saturation (SaO2), he said. A normal SaO2 implies a mild disorder such as exercise-induced bronchospasm, while an abnormal SaO2 implies moderate to severe cardiopulmonary disease if dyspnea occurs at rest, mild to moderate cardiopulmonary disease if dyspnea occurs during exercise, or sleep-disordered breathing if it occurs with sleep.

Dr. Good observed that many of his cardiology colleagues routinely obtain an electrocardiogram in their patients who are short of breath, which is an important part of the work-up, but that they overlook spirometry.

"If a patient has dyspnea they need to have spirometry," he said. "You have to start with that. It is absolutely key."

Dyspneic patients with normal spirometry are unlikely to have significant underlying COPD or interstitial lung disease (ILD), but they could have exercise-induced bronchospasm, mild or persistent asthma, or vocal cord dysfunction.

If an obstructive pattern is observed on spirometry, this could be a clue to evaluate for COPD or asthma. A restrictive pattern on spirometry should raise suspicion for ILD, neuromuscular disease, chest wall abnormalities, pleural effusion, or heart failure, he said.

Dr. Good presented several cases that highlighted the importance of a thorough work-up, including that of a 70-year-old retired engineer with increasing air hunger dyspnea on exertion. Spirometry revealed a normal forced expiratory volume in 1 second of 2.74 L, or 84% of predicted volume, and forced expiratory vital capacity of 4.91 L, or 111% of predicted volume. The FEV1/FVC ratio was 56%, which is low, but not enough to explain the amount of dyspnea the patient was experiencing. Cardiac evaluation proved uneventful, but pulmonary function tests revealed a diffusion capacity of 17.2, or just 53% of predicted value.

Dr. Good said that pulmonologists frequently rely on diffusion capacity when spirometry is normal, and when values are less than 50% of predicted, patients are frequently dyspneic.

"Once the dyspnea evaluation is complete, it is usually possible to determine all factors that are contributing to the patient’s breathlessness and direct specific therapy" to the underlying disease process, he said.

Other therapeutic approaches include conditioning, fitness, and weight loss in obese patients with dyspnea, as well as beta-agonists and anticholinergics, theophylline, opiates, anxiolytics, and selective serotonin reuptake inhibitors. Supplemental oxygen usually relieves dyspnea in hypoxemic patients, making vagal afferents unlikely contributors, he said.


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