N. R. ANTHONISEN, M.D.; H. J. SMITH, M.D.
Hyperventilation manifested by a low arterial carbon dioxide pressure (PaCO2) is a common feature of pulmonary venous congestion (1-3). This is also commonly the case in frank pulmonary edema, when significant lowering of arterial oxygen saturation (SaO2) may also be present (3, 4). However, severe pulmonary edema imposes considerable mechanical restriction on the lungs (5, 6), and it would not be surprising if hypoventilation became a problem in such instances. Indeed, several patients have been reported showing mild carbon dioxide retention (4, 7), and it has been said that PaCO2 rises sharply in the terminal stages of pulmonary edema (2).
N. R. ANTHONISEN, H. J. SMITH. Respiratory Acidosis as a Consequence of Pulmonary Edema. Ann Intern Med. 1965;62:991–999. doi: 10.7326/0003-4819-62-5-991
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Published: Ann Intern Med. 1965;62(5):991-999.
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