Clinical Disturbances Of Acidbase Balance

In understanding the physiologic mechanisms that normally regulate acid-base balance with dietary intake and metabolic production of acids and bases, it is helpful to examine the common acid-base disturbances. These conditions show the various ways in which acid-base imbalances can develop and how physiologic control mechanisms operate to restore the plasma H+ concentration as close to normal as possible. In considering these examples, it should also be realized that normal acid-base balance does not merely mean the presence of a normal plasma pH. As can be seen from the Henderson equation (Eq. [8]), an H+ concentration of 40 nmol/L could occur with an unlimited number of Pco2 and HCO— values, as long as the ratio of Pco2 to HCO— remains 40:24 = 1.67. For example, a patient might have metabolic alkalosis because of severe vomiting, which increases his or her plasma HCO— concentration to 36 mmol/L, and a simultaneous respiratory acidosis with a PCO2 of 60 mm Hg caused by inadequate respiratory ventilation (e.g., because of the simultaneous presence of pneumonia). The calculated H+ concentration of 40 nmol/L (pH 7.4) suggests that the patient has no acid-base disturbance, whereas in fact he or she has coexisting metabolic alkalosis and respiratory acidosis. For this reason, it is important to make the distinction between an elevated plasma hydrogen ion concentration (which is referred to as acidemia) and acidosis, which may or may not involve acidemia. Similarly, alkalemia should be distinguished from alkalosis.

Acid-base changes can be discussed most easily in terms of their effect on the mass balance between H+, HCO—, and CO2 in the equilibrium reactions for the HCO—/CO2 buffer system (Eq. [1]). In other words, when the concentration of one of the reactants or

Liver

Extracellullar Urea Glutamine space

Kidney

Urine

Urea

FIGURE 5 Excretion of ammonium in the urine spares plasma bicarbonate. Metabolism of amino acids in the liver results in the production of NH4+ and HCO-. These products can be used to form either glutamine or urea, which is excreted by the kidney. When glutamine is utilized by gluconeogenic pathways in the kidney, NH4+ and a-ketoglutarate are produced. The NH4+ is excreted in the urine, whereas HCO- is returned to the plasma to buffer hydrogen ions produced by metabolism of amino acids and lipids. Thus, the utilization of glutamine by the kidneys allows excretion of NH4+ from amino acid metabolism and spares plasma HCO- that would be otherwise consumed in ureagenesis. The normal metabolism of phospholipids and proteins (right side of figure) leading to the production of strong fixed acids is indicated. The anions of these strong acids are excreted in the urine and contribute to the titratable acidity.

Urea

FIGURE 5 Excretion of ammonium in the urine spares plasma bicarbonate. Metabolism of amino acids in the liver results in the production of NH4+ and HCO-. These products can be used to form either glutamine or urea, which is excreted by the kidney. When glutamine is utilized by gluconeogenic pathways in the kidney, NH4+ and a-ketoglutarate are produced. The NH4+ is excreted in the urine, whereas HCO- is returned to the plasma to buffer hydrogen ions produced by metabolism of amino acids and lipids. Thus, the utilization of glutamine by the kidneys allows excretion of NH4+ from amino acid metabolism and spares plasma HCO- that would be otherwise consumed in ureagenesis. The normal metabolism of phospholipids and proteins (right side of figure) leading to the production of strong fixed acids is indicated. The anions of these strong acids are excreted in the urine and contribute to the titratable acidity.

TABLE 4 Excretion of Titratable Acidity and Ammonium

Total acid excreted (mmol/day)

Ratio of NH4+ to titratable acidity

Normal diet:

Total acid excreted (mmol/day)

Normal diet:

ammonium

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