To the fundamental studies of Sir James MacKenzie we are indebted for the concept that in cardiac disease the patient's response to effort constitutes the best index to prognosis and the most accurate guide to therapy. Although most clinicians would agree that the patient's dyspnea, that is, his subjective respiratory distress, is the most important clinical phenomenon in cardiac disease, an adequate explanation of the mechanism of this symptom has yet to be offered.
The generally accepted idea of respiratory control involves the assumption that any muscular effort that is sufficiently severe to increase the ventilation is necessarily associated with shifts toward acidity in the blood or in the respiratory center itself. According to Haldane,1 Winterstein2 and numerous other authors, the activity of the respiratory center is dependent almost entirely on the hydrogen ion concentration of the arterial blood. The recent studies of Gesell3 have demonstrated the
HARRISON TR, HARRISON WG, CALHOUN JA, MARSH JP. CONGESTIVE HEART FAILURE: XVII. THE MECHANISM OF DYSPNEA ON EXERTION. Arch Intern Med (Chic). 1932;50(5):690–720. doi:10.1001/archinte.1932.00150180043004
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