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Arterial blood pH

Figure 30-11

Acid-base nomogram showing arterial blood pH, arterial plasma HCO3-, and Pco2 values. The central open circle shows the approximate limits for acid-base status in normal people. The shaded areas in the nomogram show the approximate limits for the normal compensations caused by simple metabolic and respiratory disorders. For values lying outside the shaded areas, one should suspect a mixed acid-base disorder. (Adapted from Cogan MG, Rector FC Jr: Acid-Base Disorders in the Kidney, 3rd ed. Philadelphia: WB Saunders, 1986.)

consistent with a mixed acid-base disturbance consisting of metabolic acidosis as well as a respiratory component.

The acid-base diagram serves as a quick way to assess the type and severity of disorders that may be contributing to abnormal pH, Pco2, and plasma bicarbonate concentrations. In a clinical setting, the patient's history and other physical findings also provide important clues concerning causes and treatment of the acid-base disorders.

Use of Anion Gap to Diagnose Acid-Base Disorders

The concentrations of anions and cations in plasma must be equal to maintain electrical neutrality. Therefore, there is no real "anion gap" in the plasma. However, only certain cations and anions are routinely measured in the clinical laboratory. The cation normally measured is Na+, and the anions are usually Cl- and HCO3-. The "anion gap" (which is only a diagnostic concept) is the difference between unmeasured anions and unmeasured cations, and is estimated as

The anion gap will increase if unmeasured anions rise or if unmeasured cations fall. The most important unmeasured cations include calcium, magnesium, and potassium, and the major unmeasured anions are albumin, phosphate, sulfate, and other organic anions. Usually the unmeasured anions exceed the unmeasured cations, and the anion gap ranges between 8 and 16 mEq/L.

The plasma anion gap is used mainly in diagnosing different causes of metabolic acidosis. In metabolic aci-

Table 30-4

Metabolic Acidosis Associated with Normal or Increased Plasma Anion Gap

Increased Anion Gap (Normochloremia)

Diabetes mellitus (ketoacidosis) Lactic acidosis Chronic renal failure Aspirin (acetylsalicylic acid)

poisoning Methanol poisoning Ethylene glycol poisoning Starvation

Normal Anion Gap (Hyperchloremia)

Diarrhea

Renal tubular acidosis Carbonic anhydrase inhibitors Addison's disease dosis, the plasma HCO3- is reduced. If the plasma sodium concentration is unchanged, the concentration of anions (either Cl- or an unmeasured anion) must increase to maintain electroneutrality. If plasma Cl-increases in proportion to the fall in plasma HCO3-, the anion gap will remain normal, and this is often referred to as hyperchloremic metabolic acidosis.

If the decrease in plasma HCO3- is not accompanied by increased Cl-, there must be increased levels of unmeasured anions and therefore an increase in the calculated anion gap. Metabolic acidosis caused by excess nonvolatile acids (besides HCl), such as lactic acid or ketoacids, is associated with an increased plasma anion gap because the fall in HCO3- is not matched by an equal increase in Cl-. Some examples of metabolic aci-dosis associated with a normal or increased anion gap are shown in Table 30-4. By calculating the anion gap, one can narrow some of the potential causes of metabolic acidosis.

References

Alpern RJ: Renal acidification mechanisms. In Brenner BM (ed):The Kidney, 6th ed. Philadelphia:WB Saunders, 2000, pp 455-519.

Capasso G, Unwin R, Rizzo M, et al: Bicarbonate transport along the loop of Henle: molecular mechanisms and regulation. J Nephrol 15(Suppl 5):S88, 2002.

Decoursey TE: Voltage-gated proton channels and other proton transfer pathways. Physiol Rev 83:475, 2003.

Gennari FJ, Maddox DA: Renal regulation of acid-base homeostasis. In Seldin DW, Giebisch G (eds): The Kidney—Physiology and Pathophysiology, 3rd ed. New York: Raven Press, 2000, pp 2015-2054.

Good DW: Ammonium transport by the thick ascending limb of Henle's loop. Ann Rev Physiol 56:623,1994.

Igarashi I, Sekine T, Inatomi J, Seki G: Unraveling the molecular pathogenesis of isolated proximal renal tubular aci-dosis. J Am Soc Nephrol 13:2171, 2002.

Karet FE: Inherited distal renal tubular acidosis. J Am Soc Nephrol 13:2178, 2002.

Laffey JG, Kavanagh BP: Hypocapnia. N Engl J Med 347:43, 2002.

Lemann J Jr, Bushinsky DA, Hamm LL: Bone buffering of acid and base in humans. Am J Physiol Renal Physiol 285:F811, 2003.

Madias NE, Adrogue HJ: Cross-talk between two organs: how the kidney responds to disruption of acid-base balance by the lung. Nephron Physiol 93:61, 2003.

Wagner CA, Geibel JP: Acid-base transport in the collecting duct. J Nephrol 15(Suppl 5):S112, 2002.

Wesson DE, Alpern RJ, Seldin DW: Clinical syndromes of metabolic alkalosis. In Seldin DW, Giebisch G (eds): The Kidney—Physiology and Pathophysiology, 3rd ed. New York: Raven Press, 2000, pp 2055-2072.

White NH: Management of diabetic ketoacidosis. Rev Endocr Metab Disord 4:343, 2003.

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