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JAMA. 1965;192(9):778-779. doi:10.1001/jama.1965.03080220042015.
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Two mechanisms are generally proposed to explain the retention of carbon dioxide in obstructive pulmonary disease. One holds that abnormal ventilatory control leads to alveolar hypoventilation and thence to hypercapnia, and that some reversal of arterial carbon dioxide partial pressure (Pco2) might be expected under conditions of hyperventilation. Another explanation is that carbon dioxide retention is an inevitable accompaniment of severe disease with or without abnormal ventilatory control, and that little or no reversal can be expected. The extent to which these mechanisms are operating will help to establish the rationale and intensity of ventilation therapy. One means of examining this problem is to test the effects of voluntary hyperventilation in suitable patients, as Gilbert et al have done recently.1

Pulmonary-function studies, at rest and during exercise, were performed in 30 men with chronic obstructive pulmonary disease, aged 32 to 51 years. Carbon dioxide retention was directly related


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