Dyspnea Definition Dyspnea, a major cause of distress and disability in cardiac patients, is one of the most important symptoms of heart disease. Yet it is one of the least understood, partly because it is inherently subjective in nature and hence difficult to measure and partly because no single class of receptors, discrete pathway, or mechanism has been found that can account for dyspnea in all the myriad settings in which it occurs. Indeed, despite many decades of investigation summarized in several excellent symposia, there is not even universal agreement concerning the definition of dyspnea, although it is commonly regarded as "shortness of breath or an unpleasant intrusion of the normally subconscious sensation of breathing into the conscious domain. It is most commonly seen in patients with disease of the heart or lungs and in patients with mechanical dysfunction of the respiratory apparatus, including the lungs, chest wall, and respiratory muscles. Most would agree that in such patients shortness of breath at rest or during low-level muscular exercise constitutes dyspnea. It is less obvious whether the term dyspnea could also be applied to the respiratory distress experienced by normal individuals during maximal or near-maximal exercise or at the break point of a breath hold. In these cases the term breathlessness is often used. Whether the sensation is labeled "dyspnea" or "breathlessness" may depend on whether it is perceived as appropriate or inappropriate to the level of activity. In the case of dyspnea, the respiratory distress seems disproportionate to the degree of activity, and thus is considered pathologic, whereas in breathlessness the sensation is appropriate to the respiratory demands, as in heavy exercise. A few other terms should be defined at the outset. These include hyperpnoea, the classic response to exercise, in which ventilation increases according to metabolic demands, and, as a result, blood gas tensions, particularly CO2 tension, remain constant. Hyperventilation, in contrast, refers to increases in ventilation that are dis-proportionate to metabolic demands and thus lead to decreases in arterial CO2 tension. Tachypnea denotes a shift in respiratory pattern to an increased respiratory rate and a decreased tidal volume. All of these objective aspects of ventilation are frequently associated with dyspnea, but, unlike dyspnea, they constitute measurable signs. Physiology Dyspnea is in many respects analogous to pain: both are symptoms produced by noxious stimuli, both are subjective warnings that something is wrong, and both may be protective. Pain serves to limit motion in an injured extremity, and dyspnea may serve to limit exertion, thus preserving the balance of gas exchange and metabolic demand. It may also minimize respiratory muscle fatigue. Finally, dyspnea may be a factor in a feedback loop that results in optimal respiratory breathing strategies that, in turn, reduce dyspnea—an analog of the way in which pain in an extremity may lead a person to alter his gait to minimize pain. Unlike pain, however, dyspnea has thus far not been associated with any single class of stimuli or receptors, nor have discrete pathways or central nervous system (CNS) centers analogous to those mediating pain been described for dyspnea. Indeed, a unifying theory that accounts for stimuli, pathways, and mechanisms of dyspnea and that satisfactorily explains how and why dyspnea arises in so many clinical settings has not been found. Still, a pathogen etic scheme can be formulated that explains many of the characteristics of dyspnea and is helpful in understanding its features. Respiratory Dysfunction Ventilatory dysfunction leading to decreased ventilatory capacity is common to a large proportion of patients complaining of dyspnea. Dysfunction can be due to increased airways resistance, as in airways obstruction; to decreased lung compliance, as in restrictive lung disease; to changes in the shape or compliance of the chest wall; to weakness of the respiratory muscles; or to inefficient ventilation caused by alterations in dead space or ventilation-perfusion imbalance. Ventilatory Capacity-Demand Imbalance It is clear that, in addition to dysfunction of the respiratory apparatus, other factors must be considered as, for example, in the case of a patient who breathes easily at rest but in whom profound dyspnea is induced by mild exercise. Hypoxia, hypercapnia, and acidosis, which act to increase ventilation, elicit a similar sensation, which suggests that dyspnea is more the result of an unfavorable relationship between ventilatory capacity and ventilatory demand than of decreased capacity alone. Decreased capacity may be well tolerated when ventilatory demands are low but may lead to dyspnea in the face of even modest increases in ventilatory requirements. Exercise is by far the most common stress leading to increased dyspnea in patients with respiratory dysfunction, and it should be regularly inquired about during history taking. The answers to questions about, for example, how many flights of stairs the patient can climb or the distance he or she can walk on level ground before experiencing disabling dyspnea provide useful semi quantitative information. In addition to exercise, a number of other ventilatory drives may also work to increase ventilatory demand and contribute to the development of dyspnea. These include hypoxemia, which may result from lung disease or from sojourn at high altitude, and acidosis, either respiratory or metabolic, which is a classic stimulus to breathing and may precipitate or augment dyspnea in patients with respiratory dysfunction.