Although the phenomenon of severe acidosis in the depressed neonate is now widely appreciated, our understanding of both pathogenesis and clinical significance of this disturbance is still incomplete. The fall in blood pH under such circumstances is usually due to accumulation of both carbon dioxide and titratable non-volatile acid; the latter feature is explained in part by bicarbonate redistribution in response to hypercapnia and in part by addition to the blood of organic acid in response to hypoxia. In the hypoxic infant, elevations of the blood lactate level often fall short of the change in the concentration of blood titratable acid as reflected by the blood "base excess;"1,2 and, in recent experimental studies on this problem we found that, in (constantly) normocapnic dogs, acute severe hypoxia leads to a rapid fall in blood "base excess" before any appreciable rise in lactate levels occurs. Because conventional "physiological-type" acid-base terminological systems do not allow for the presence of secondary noncompensatory variables, the "high Pco2-low base excess" type of acidosis so characteristic of the asphyxiated newborn is not easily classifled in terms of conventional acid-base diagnostic categories. Far from representing a "misinterpretation of negative "base excess values," as stated by Nelson and Riegel, classification of this particular disturbance as a "mixed acidosis" appears reasonable in view of the evidence described in the foregoing; actually, the identical diagnostic attitude is implicit in Nelson and Riegel paper. On the other hand, we wish to emphasize that both bicarbonate redistribution and accumulation of organic acids are secondary to the primary pulmonary insufficiency, and that both are rapidly reversible upon restoration of adequate pulmonary function.
Purely periodic expansions in systems with negative base
