For many years there has been a great interest in the mechanism of dyspnea in patients with heart disease. Our present concepts of the nature of dyspnea are largely attributable to the careful studies of Francis Peabody.1-3 He demonstrated that patients with severe heart failure had an increase in the minute volume of respiration at rest. The rate of breathing was increased, and the tidal volume was small, resulting in an increased ventilation of dead space. Patients with heart failure exhibited a greater increase in ventilation for a given degree of exercise than did normal persons. Peabody emphasized that this increase in ventilation at rest or on exercise did not in itself explain the dyspnea of heart failure. Patients with heart disease complained of discomfort at a level of ventilation which caused no unusual sensation in normal persons. This tendency to dyspnea was closely related to the magnitude
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