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Dyspnea

Richard Morrison & Warren R. Summer

OBJECTIVES

Define dyspnea and its pathophysiologic relationship to various disease processes.

Identify types of respiratory disease by the recognition of spirometric patterns.

Identify appropriate tests used in the systematic evaluation of dyspnea.

GENERAL CONSIDERATIONS

Dyspnea is a sensation of breathlessness or subjective “shortness of breath.” It defies strict definition with many individual descriptions and varies widely among patients for comparable objective dysfunction. The American Thoracic Society (ATS) has defined dyspnea as “a term used to characterize a subjective experience of breathing discomfort that is comprised of quantitatively distinct sensations that vary in intensity.” The sensation of breathlessness can be experienced by healthy subjects with exercise or at high altitudes and those with diseases that affect the respiratory, cardiac, endocrine, renal, neurologic, hematologic, or rheumatologic systems. It is a frequent clinical complaint. Occasionally, a source cannot be clearly identified, and dyspnea is attributed to psychophysiologic disturbances.

ETIOLOGY & PATHOGENESIS

Dyspnea in patients with chronic obstructive pulmonary disease (COPD) is due to narrowing of the airways, increased airway resistance, and reduction of lung elastic recoil. Very often, concominant hyperinflation is seen, which alters respiratory muscle mechanics, thereby increasing the sensation of dyspnea. Infiltration of the lung parenchyma in diffuse lung disease such as pulmonary fibrosis can also result in similar ventilatory impediment due to increased elastic work of breathing. This is also seen in conditions causing acute respiratory distress syndrome (ARDS) and pulmonary edema with congestive heart failure (Table 1–1). Excessive secretions and inability to clear such secretions can compromise airways and increase airway resistance. Chest wall mechanics can also be compromised by pleural disease and cause dyspnea. Some patients with chronic lung disease have increased minute ventilation at rest and on exertion due to increased dead space (wasted ventilation), increased carbon dioxide production, and enhanced drive to breathe.

The sensation of dyspnea increases when the demand to breathe is disproportionate to the requirement. Increased work of breathing resulting from an imbalance between afferent inputs and respiratory muscle output due to poor nutrition and muscle strength can contribute to the sensation of dyspnea. Common to the processes causing metabolic acidosis, such as aspirin, methanol ingestion, increased lactic acidosis due to poor tissue perfusion, overproduction of ketones secondary to metabolism of fatty acids (eg, diabetic ketoacidosis, alcoholism, or starvation), renal failure (decreased excretion of hydrogen ions), or bicarbonate loss (eg, diarrhea, renal dysfunction, or pancreatic disease), is an increase in hydrogen ions, which stimulate arterial receptors, especially those in the carotid bodies. This respiratory compensation is often appreciated or perceived as dyspnea.

PATHOPHYSIOLOGY & MECHANISM OF DYSPNEA

Breathing is an unconscious act; we are only aware of our breathing effort when something is wrong. Many respiratory conditions can present acutely with the sensation of dyspnea. Dyspnea is not a single sensation and the mechanism of dyspnea is not well understood. Similar to pain, dyspnea appears to be multidimensional encompassing unpleasantness and emotional impact. Dyspnea has two dimensions, sensory and affective, and both can be independently identified in the laboratory and in clinical situations. Also, it is a perception or subjective experience and it must be explained by human experiments. New brain imaging studies indicate that the sensation of different respiratory efforts is perceived in several areas of the brain stem and sensory cortex with dyspnea resulting when the degree of stimulation in respiratory-related neurons is perceived as being excessive. Stimulation may arise from different situations (eg, exercise, hypoxia, or breath-holding), medical conditions (eg, increased airway resistance, decreased compliance, or increased work of breathing), physical discomfort (pain), metabolic changes (acidosis), emotional discomfort, excitement, and depression. Receptors in the heart may also give rise to perceptions of dyspnea (orthopnea) since awareness of breathing may occur with apparently normal lungs and gas exchange.

Table 1–1. Pathophysiologic correlates of disease causing dyspnea

The increased afferent stimulation of the respiratory complex from a variety of receptors (chemoreceptors, proprioreceptors, or emotions) results in increasing efferent neural drive to the respiratory muscles. Additional stimuli of other afferent pathways can contribute (eg, bronchospasm, inflammation, pulmonary hypertension, or lung edema). This information is simultaneously relayed to sensory areas within the cortex.

An understanding of basic respiratory physiology enables the clinician to categorize and evaluate dyspnea. Basic concepts such as increased respiratory drive, respiratory muscle weakness, dead space ventilation, and mechanical impairment of ventilation, all contribute to an understanding of the underlying causes and mechanisms of dyspnea. It is possible to narrow the differential diagnosis and evaluation of dyspnea by asking whether the symptoms are acute or chronic (see Figures 1–1 and 1–2). Acute changes are more likely to be seen in congestive heart failure, myocardial infarction, exacerbations of COPD, asthma attacks, pulmonary embolism, and pneumonia. Dyspnea is usually recognized as chronic when it is present for at least 4–8 weeks. Common causes and observed frequencies for chronic dyspnea are listed in Table 1–2.

Evaluation of the History

A comprehensive history is required and will help to define the timing, precipitating or aggravating factors, related conditions, severity of symptoms, their relationship to activity, and any identifiable alleviating factors. Patients with certain diseases tend to describe the shortness of breath in similar terms (Table 1–3), but the reliability of specific descriptions is suspect. Nocturnal dyspnea may be related to several disease processes, such as asthma, congestive heart failure, gastroesophageal reflux, or nasal congestion. In the supine position, dyspnea may be related to something that upwardly displaces the abdominal contents, such as pregnancy, ascites, diaphragmatic paralysis, or redistribution of intravascular volume to the central circulation that is not compensated due to a failing heart. If symptoms are intermittent, the clinician should consider reversible diseases such as asthma (bronchoconstriction), heart failure, or recurrent pulmonary emboli. Progressive symptoms usually signal more chronic diseases, such as interstitial pulmonary fibrosis, sarcoidosis, COPD, amylotrophic lateral sclerosis, or cancer.

Table 1–2. Frequency (%) of respiratory conditions presenting to an emergency department with a chief complaint of breathlessness

Table 1–3. Often-used patient descriptions of dyspnea as reported in asthma

Table 1–4. American Thoracic Society shortness of breath scale

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