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Joseph L. Grant, MD
Arch Intern Med. 1981;141(6):819. doi:10.1001/archinte.1981.00340060127042.
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To the Editor.  —Dr Sander et al, in the March issue of the Archives (1980; 140:420-421), reported that their patient with hypoventilation caused by amyotropic lateral sclerosis could reduce his arterial Pco2 from 70 to 42 mm Hg and stated that by using accessory respiratory muscles, this patient could, like idiopathic hypoventilators, hyperventilate voluntarily to normal Pco, values. In theory, though, a true idiopathic hypoventilator (no lung disease, no nerve or muscle disorder, but a medullary center unresponsive to carbon dioxide excess) should be able to hyperventilate as does a normal subject, ie, to a range of 11 to 27 mm Hg.1,2 If the patient of Sander et al could really hyperventilate normally from an initial Pco2 of 70 mm Hg and pH of 7.32, when he achieved a Pco2 of 20 mm Hg, his pH would be 7.7. Although one characteristic of idiopathic hypoventilators


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