gap. This approach uses only the carbonic acid/bicarbonate buffer system to assess acid-base disorders and is the approach that will be used in this chapter. The two other approaches to acid-base disorders are the base excess approach and the physicochemical approach (Stewart approach). The former analysis takes into consideration all buffer systems in the body, whereas the latter approach measures the variables of strong ion difference and weak acid concentration. These two approaches have been reviewed extensively (3) and will not be discussed further in this chapter.
respiratory acidosis. In the proximal tubule, increases in PaCO2 cause corresponding activation of the luminal Na/H exchanger and basolateral Na/HCO3 exchanger, leading to net reabsorbtion of bicarbonate (9). There also appears to be increased activity of H+/ATPase in the distal tubule (10). The chemical buffering and renal compensation that occur with chronic respiratory acidosis are diagramed in Figure 4-1.
acidosis is characterized by an elevation of the plasma [HCO3–] by about 1 mmol/L (>24) for each 10 mm Hg acute increment in PaCO2 (>40) (12):
a holding measure to prevent the serious cardiovascular effects of marked acidemia until definitive therapy is established (20). Because equilibration of HCO3– across the blood-brain barrier is markedly slower than that of CO2 with bicarbonate administration, a delay in the correction of the cerebral pH may occur, and cerebrospinal fluid pH falls initially (21).
Table 4-1 Causes of Acute Respiratory Acidosis
Table 4-2 Causes of Chronic Respiratory Acidosis