Breathing discomfort or significant breathlessness is a serious problem for many persons in the U.S. Approximately 14 million Americans suffer from chronic obstructive pulmonary disease (COPD). Another 10 million citizens (approximately five percent of the population) have asthma. When interstitial lung disease, neuromuscular disorders, lung cancer, and cardiac disease are added to the mix, it is clear that many people suffer from the difficult, labored, uncomfortable breathing known as dyspnea.

The January issue of the American Journal of Respiratory and Critical Care Medicine includes a consensus statement on dyspnea
by 18 experts from the American Thoracic Society which was endorsed by the ATS Board of Directors.  A unifying theory about dyspnea or significant breathlessness is that itresults from a mismatch between central respiratory motor activity and the incoming information from receptors in the airways, lungs, and chest wall structures. This disassociation between the motor command and
the mechanical response of the respiratory system frequently produces a sensation of respiratory discomfort that afflicts millions
of people.  As pointed out in this consensus statement, respiratory diseases such as COPD and asthma, which narrow airways
and increase airway resistance, as well as diseases of the functional part of the lung such as pulmonary fibrosis, commonly cause dyspnea. However, dyspnea, like hunger or thirst, is largely a sensation which arises from multiple sources rather that from stimulation of a single neural receptor. Also, the severity of dyspnea, as well as the sensation of breathlessness, varies widely
among patients.

In many cases, the primary problem behind dyspnea involves heart, lung, or neuromuscular abnormalities, which physicians identify by taking a history and doing a physical exam. Then doctors focus on the symptoms of breathlessness, including trying to determine quality, intensity, duration, frequency, and the amount of distress or discomfort. In the statement, physicians are urged to distinguish between two broad categories:

conditions associated with cardiovascular dyspnea involving inadequate oxygen delivery to the tissues; and pulmonary dyspnea or conditions associated with a heightened respiratory drive, altered pulmonary mechanisms, or gas exchange abnormalities. Sometimes
the problem involves a combination of symptoms associated with two major illnesses such as COPD and congestive heart failure.  According to the consensus statement, even after dealing with the underlying problem such as heart disease, the patient often continues to experience significant breathlessness. Many of the therapeutic interventions suggested by this consensus statement relieve dyspnea by addressing different pathophysiologic mechanisms in the body, such as improving respiratory muscle function and altering central perceptions of the problem.

These include:

1.  Exercise Training
Controlled studies have shown that dyspnea upon exertion decreases and exercise tolerance improves in response to exercise training, even in patients with advanced disease. It is now well established that for patients with COPD who remain breathless despite optimal drug therapy, exercise training can confer significant symptomatic benefits.

2.  Pharmacologic Therapy
Two types of medications have proven useful in alleviating dyspnea: opiates and drugs that reduce anxiety. A number of studies have shown that opiates acutely relieve dyspnea and improve exercise performance in patients with COPD. The drugs to reduce anxiety
have the potential to relieve ventilatory response related to the available amounts of oxygen in the blood, as well as by lowering the emotional response to dyspnea.

3.  Fans
The movement of cool air with a fan has been observed to reduce dyspnea in pulmonary patients. A decrease in the temperature of the facial skin alters feedback to the brain and modifies the perception of dyspnea. Cool air has been shown in normal volunteers to reduce dyspnea in response to excess carbon dioxide in the blood.

4.  Altered Breathing Patterns
Breathing retraining including diaphragmatic breathing and pursed lip breathing has been advocated to relieve dyspnea in COPD patients.  During a breathing retraining period, many patients adopt slower, deeper breathing techniques; however, they often resort
to spontaneous, fast, shallow breathing patterns when the training ends.

5.  Continuous Positive Airway Pressure (CPAP)
In various studies, CPAP has been shown to relieve dyspnea during asthma attacks, when patients are being weaned from ventilators, and during exercise sessions for patients with advanced COPD.

6.  Nutrition
Several investigators have shown improvement in respiratory muscle function in response to short-term use of nutritional repletion by an intravenous route.

7.  Positioning
Patients with COPD often change body position to improve dyspnea. They tend to lean forward to improve overall respiratory muscle strength and to reduce their symptoms.

8.  Steroids
Steroid use can be beneficial to pulmonary patients by reducing airway inflammation and by increasing vital capacity in chronic lung
inflammation.  However, steroids have adverse effects, including muscle wasting and weakness. These potential problems need to be
balanced against possible gains in lung function associated with this drug.  Cognitive-behavioral Approaches In patients with different pain syndromes, distraction, relaxation, and education about symptoms have modified the intensity of pain, increased tolerance, and decreased distress. Improvements in dyspnea and anxiety have been shown to follow distractions such as music during exercise, although long-term effects have been minimal. However, exercise in a monitored, supportive environment has been shown to be a powerful method of overcoming apprehension, anxiety, and/or fear associated with exertional dyspnea.

Pulmonary thromboembolism produces arterial hypoxemia due to mismatched ventilation (which remains largely normal) and perfusion (which is reduced in the region of lung supplied by the occluded artery). Vasoconstriction of the affected artery results in shunting of blood flow to other, unaffected regions of lung, at the price of some degree of pulmonary hypertension.  Additionally, most patients with acute PE develop acute respiratory alkalosis due to an increase in minute ventilation.  This is manifest clinically as rapid breathing (tachypnea).  Some patients do experience chest pain, usually of a pleuritic nature (though it can mimic acute MI, as well), but patients do not usually note increased work of breathing (i.e., increased effort), or incomplete exhalation or chest tightness (in contrast to asthma).