contain many proteins and organic phosphates that can bind H + . For example, hemoglobin (Hb) in red blood cells combines with H+ from H2CO3, minimizing the increase in free H + . Recall from Chapter 21 the buffering reaction:

H2CO3 + HbO2

This reaction raises the plasma [HCO3_]. In acute respiratory acidosis, such chemical buffering processes in the body lead to an increase in plasma [HCO3~] of about 1 mEq/L for each 10 mm Hg increase in Pco2 (see Table 25.4). Bicarbonate is not a buffer for H2CO3 because the reaction

is simply an exchange reaction and does not affect the pH.

An example illustrates how chemical buffering reduces a fall in pH during respiratory acidosis. Suppose Pco2 increased from a normal value of 40 mm Hg to 70 mm Hg ([CO2(d)] = 2.l mmol/L). If there were no body buffer bases that could accept H+ from H2CO3 (i.e., if there was no measurable increase in [HCO3_]), the resulting pH would be 7.16:

Renal Compensation. The kidneys compensate for respiratory acidosis by adding more H+ to the urine and adding new HCO3~ to the blood. The increased Pco2 stimulates renal H+ secretion, which allows the reabsorption of all filtered HCO3~. Excess H+ is excreted as titratable acid and NH4+; these processes add new HCO3~ to the blood, causing plasma [HCO3~] to rise. This compensation takes several days to fully develop.

With chronic respiratory acidosis, plasma [HCO3~] increases, on average, by 4 mEq/L for each 10 mm Hg rise in Pco2 (see Table 25.4). This rise exceeds that seen with acute respiratory acidosis because of the renal addition of HCO3~ to the blood. One would expect a person with chronic respiratory acidosis and a Pco2 of 70 mm Hg to have an increase in plasma HCO3~ of 12 mEq/L. The blood pH would be 7.33:

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