Respiratory acidosis resulting from carbon dioxide retention which complicates obstructive lung disease has been extensively investigated during the past two decades. Its therapy now commands a wide range of techniques and apparatus which have become standard equipment in most hospitals. Metabolic acidosis caused by lactate accumulation in the blood during hypoxia is well recognized.1 Less well appreciated are the recently described respiratory acidosis and metabolic (lactate) acidosis which complicate pulmonary edema.
In 1965 Anthonisen and Smith2 reported on four patients with acute pulmonary edemia in whom both respiratory and metabolic acidosis were sufficiently severe to require treatment. They suggested that respiratory acidosis was caused by carbon dioxide retention due to airway obstruction or collapse by edema fluid, and that concomitant metabolic acidosis was due to lactate accumulation secondary to hypoxia in poorly perfused tissue. A later report by Agostoni3 noted both metabolic and respiratory acidosis—the former predominating—in