The terms cardiac dyspnea, dyspnea related to lung disease, and renal dyspnea originated in the nineteenth century, when it was first firmly established that dyspnea was associated with morbid anatomical changes in the heart, lung, and kidneys; when no abnormality was detected, then dyspnea was considered neurogenic. At that time conjecture about mechanism was of little practical importance because amelioration of the heart or lung disorder was the only requirement for management, and some would argue that this remains true today. In a similar fashion, dyspnea was not a topic of particular interest to physiologists. Their real interest was in the physiology of respiration. Nonetheless, tacit assumptions about the mechanism of dyspnea emerged. Hence, it is not surprising that hypoxia, hypercapnia, and acidemia were successively put forward as the mechanisms of dyspnea. Common experience revealed that when the breath is voluntarily held, an unpleasant urge to breathe emerges, attributed to chemoreceptor activation. This constituted the chemical theory (Pfluger, 1868; Miescher-Rusch, 1885; Winterstein, 1911, 1921; Meakins, 1923; Gesell, 1923; Haldane and Smith, 1935). The neurophysio1ogists adopted a somewhat different standpoint; they saw central medullary respiratory neuronal activity contributing to dyspnea (LeGallois, 1812). Later they saw lung expansion hindered by stiffness consequent on disease contributing to failure of the

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self-steering reflex, described by Hering and Breuer (Breuer and Hering, 1868), to inhibit medullary inspiratory neuronal activity, thereby causing dyspnea (Gad, 1911; Wright and Branscomb, 1954). This constituted the reflex theory. The physiologists of the early twentieth century saw ventilation encroaching on ventilatory capacity as the mechanism for dyspnea (Means, 1924; Cournand et al . , 1939; Cournand and Richards, 194la,b; Cournand et al., 1941) with increased force, work, and/or oxygen debt by the respiratory muscles as stimuli (Donders, 1853; Wirz, 1923; Rohrer, 1925; Otis et al., 1950; Harrison, 1950; Marshall et al., 1954; Mcilroy, 1958; Cherniack, 1959; Aaron et al., 1991). This constituted the mechanical theory. All of these mechanisms continue to be put forward from time to time. Confusion has arisen because chemoreceptor stimulation, respiratory center output, blood gases, pulmonary mechanics, and vagal and chest wall receptor stimulation and their afferents are all integral to the process of breathing and because directly and indirectly all of these unit processes result in the stimulation of a variety of sensory receptors with access to consciousness resulting in the genesis of dyspnea. In the past 30 years dyspnea has been approached in a fundamentally different way. The integrated nature of these respiratory processes is accepted, psychophysical methods, including detection, recognition, and scaling, are now increasingly applied, and dyspnea arising in its clinical context is analyzed within the confines of respiratory and sensory physiology (for review see Killian, 1992).