Dyspnea

Dyspnea, or shortness of breath, is frequently a difficult symptom for the physician to evaluate because it is such a subjective feeling experienced by the patient. It is perhaps best defined as an uncomfortable sensation (or awareness) of one’s own breathing, to which little attention normally is paid. However, the term dyspnea probably subsumes several sensations that are qualitatively distinct. As a result, when patients are asked to describe in more detail their sensation of breathlessness, their descriptions tend to fall into three primary categories: (1) air hunger or suffocation, (2) increased effort or work of breathing, and (3) chest tightness.

Not only is the symptom of dyspnea highly subjective and describable in different ways, but the patient’s appreciation of it and its importance to the physician depend heavily on the stimulus or amount of activity required to precipitate it. The physician must take into account how the stimulus, when quantified, compares with the patient’s usual level of activity. For example, a patient who is limited in exertion by a nonpulmonary problem may not experience any shortness of breath even in the presence of additional and significant lung disease. If the person were more active, however, dyspnea would become readily apparent. A marathon runner who experiences a new symptom of shortness of breath after running 5 miles may warrant more concern than would an elderly man who for many years has had a stable symptom of shortness of breath after walking 3 blocks.

Dyspnea should be distinguished from several other signs or symptoms that may have an entirely different significance. Tachypnea is a rapid respiratory rate (greater than the usual value of 12–20/min). Tachypnea may be present with or without dyspnea, just as dyspnea does not necessarily entail the finding of tachypnea on physical examination. Hyperventilation is ventilation that is greater than the amount required to maintain normal CO₂ elimination. Hence, the criterion that defines hyperventilation is a decrease in the PCO₂ of arterial blood. Finally, the symptom of exertional fatigue must be distinguished from dyspnea. Fatigue may be due to cardiovascular, neuromuscular, or other nonpulmonary diseases, and the implication of this symptom may be quite different from that of shortness of breath.

There are some variations on the theme of dyspnea. Orthopnea, or shortness of breath on assuming the recumbent position, often is quantitated by the number of pillows or angle of elevation necessary to relieve or prevent the sensation. One of the main causes of orthopnea is an increase in venous return and central intravascular volume on assuming the recumbent position. In patients with cardiac decompensation and either overt or subclinical congestive heart failure, the increment in left atrial and left ventricular filling may result in pulmonary vascular congestion and pulmonary interstitial or alveolar edema. Thus, orthopnea frequently suggests cardiac disease and some element of congestive heart failure. However, orthopnea may be seen in other disorders. For example, some patients with primary pulmonary disease experience orthopnea, such as individuals with a significant amount of secretions who have more difficulty handling their secretions when they are recumbent. Bilateral diaphragmatic weakness may also cause orthopnea due to greater pressure on the diaphragm by abdominal contents and more difficulty inspiring when the patient is supine rather than upright.

Paroxysmal nocturnal dyspnea is waking from sleep with dyspnea. As with orthopnea, the recumbent position is important, but this symptom differs from orthopnea in that it does not occur soon after lying down. Although the implication with regard to underlying cardiac decompensation still applies, the increase in central intravascular volume is due more to a slow mobilization of tissue fluid, such as peripheral edema, than to a rapid redistribution of intravascular volume from peripheral to central vessels.

Variants that are much more uncommon are only mentioned here. Platypnea is shortness of breath when the patient is in the upright position; it is the opposite of orthopnea. Trepopnea is shortness of breath when the patient lies on his or her side. Patients with this symptom report dyspnea on either the right or left side. The symptom can be relieved by moving to the opposite lateral position.

Returning to the more general symptom of dyspnea, a number of sources or mechanisms are proposed rather than a single common thread linking the diverse responsible conditions. In particular, neural output reflecting central nervous system respiratory drive appears to be integrated with input from a variety of mechanical receptors in the chest wall, respiratory muscles, airways, and pulmonary vasculature. If central neural output to the respiratory system is not associated with the expected responses in ventilation and gas exchange, the patient experiences a sensation of dyspnea. Presumably, the relative contributions of each source differ from disease to disease and from patient to patient, and they are responsible for the qualitatively different sensations all subsumed under the term dyspnea. Detailed discussions of the mechanisms of dyspnea can be found in the references at the end of this chapter.

Studies have attempted to link dyspnea with underlying pathophysiologic mechanisms. While the correlations are not perfect, a patient’s description can help guide the clinician to the correct diagnosis. Patients who describe their breathlessness as a sense of air hunger or suffocation often have increased respiratory drive, which can be related in part to either a high PCO₂ or a low PO₂ but also can occur even in the absence of respiratory system or gas-exchange abnormalities. The sensation of increased effort or work of breathing is commonly experienced by patients who have increased resistance to airflow or abnormally stiff lungs. The sensation of chest tightness, frequently noted by patients with asthma, probably arises from intrathoracic receptors that are stimulated by bronchoconstriction. Because most disorders may produce breathlessness by more than one mechanism (e.g., asthma may have components of all three mechanisms), overlap or a mixture of these different sensations often occurs.

The differential diagnosis includes a broad range of disorders that result in dyspnea (Table 2-1). The disorders can be separated into the major categories of respiratory disease and cardiovascular disease. Dyspnea may be present in the absence of underlying respiratory or cardiovascular disease in conditions associated with increased respiratory drive, such as hyperthyroidism, or in metabolic disorders, such as mitochondrial myopathies. In addition, dyspnea may have an anxiety-related or psychosomatic origin.

The first major category consists of disorders at many levels of the respiratory system (airways, pulmonary parenchyma, pulmonary vasculature, pleura, and bellows) that can cause dyspnea. Airway diseases that cause dyspnea result primarily from obstruction to airflow, occurring anywhere from the upper airway to the large, medium, and small intrathoracic bronchi and bronchioles. Upper airway obstruction, which is defined here as obstruction above or including the vocal cords, is caused primarily by foreign bodies, tumors, edema (e.g., with anaphylaxis), and stenosis. A clue to upper airway obstruction is the presence of disproportionate difficulty during inspiration and an audible prolonged gasping sound called inspiratory stridor. The pathophysiology of upper airway obstruction is discussed in Chapter 7.

Airways below the level of the vocal cords, from the trachea down to the small bronchioles, are more commonly involved with disorders that produce dyspnea. An isolated problem, such as an airway tumor, usually does not by itself cause dyspnea unless it occurs in the trachea or a major bronchus. In contrast, diseases such as asthma and chronic obstructive pulmonary disease have widespread effects throughout the tracheobronchial tree, with airway narrowing resulting from spasm, edema, secretions, or loss of radial support (see Chapter 4). With this type of obstruction, difficulty with expiration generally predominates over that with inspiration, and the physical findings associated with obstruction (wheezing, prolongation of airflow) are more prominent on expiration.

The category of pulmonary parenchymal disease includes disorders causing inflammation, infiltration, fluid accumulation, or scarring of the alveolar structures. Such disorders may be diffuse in nature, as with the many causes of interstitial or diffuse parenchymal lung disease, or they may be more localized, as occurs with a bacterial pneumonia.

Pulmonary vascular disease results in obstruction or loss of vessels in the lung. The most common acute type of pulmonary vascular disease is pulmonary embolism, in which one or many pulmonary vessels are occluded by thrombi originating in systemic veins. Chronically, vessels may be blocked by recurrent pulmonary emboli or by inflammatory or scarring processes that result in thickening of vessel walls or obliteration of the vascular lumen, ultimately causing pulmonary arterial hypertension.