Step 3 Is compensation appropriate

Metabolic acidosis - Pco2 decreases by ~1.25 mm Hg for each 1 mmol/L fall in HC03 below 24

Metabolic alkalosis - Pco2 increases by ^0.6 mm Hg for each 1 mmol/L rise in HC03 above 24

Respiratory Acidosis

Acute: HC03 increases by ~1 mmol/L for each 10 mm Hg rise in Pco2 above 40 mm Hg

Chronic: HC03" increases by "3.5 mmol/L for each 10 mm Hg rise in Pco2 above 40 mm Hg

Respiratory Alkalosis

Acute: HC03 decreases by "2 mmol/L for each 10 mm Hg decrease in Pco2 below 40 mm Hg

Chronic: HC03" decreases by "5 mmol/L for each 10 mm Hg decrease in Pco2 below 40 mm Hg

FIGURE 8 Step 3 in a systematic analysis of acid-base status. In metabolic acid-base disorders, the respiratory center changes the minute rate of ventilation to raise the plasma PCO2 in alkalosis and lower it in acidosis. The change in PCO2 for a normal regulatory response is indicated. In respiratory acid-base disorders, the kidney compensates by changing the rate of HCO3- excretion and thus its plasma concentration. This renal compensation occurs over a period of hours and days in contrast to the extremely rapid changes in PCO2 that can occur with a change in ventilation. Thus the expected change in plasma HCO- is greater with chronic than with acute respiratory acidosis or alkalosis. (Adapted with alterations from the scheme of analysis presented in Andreoli TE. Carpenter CCG, Griggs RC, Loscalzo J, eds. Cecil essentials of medicine. Philadelphia: WB Saunders, 2001, p. 249.)

elevated above the normal 40 mm Hg if, for example, the acidemia is due to respiratory acidosis.

With any primary acid-base disturbance, the alteration in bicarbonate or Pco2 is expected to be accompanied by an offsetting change in the other parameter due to normal physiologic compensation. Step 3 of the analysis (Fig. 8) is designed to determine if the change in the other parameter is of the magnitude expected for normal compensation. Because renal compensation occurs more slowly, one should also take note from the history of the patient if the symptoms of a primary respiratory disorder have occurred acutely or chronically. Changes outside of the predicted range for the second parameter are an indication that the primary

Step 4. Examine the anion gap

Anion gap is the difference in plasma ion concentrations given by:

which is normally £ 12 mmol/L

Only a metabolic acidosis produced by accumulation of an acid with an unmeasured anion causes an anion gap >20 mmol/L

FIGURE 9 Step 4 in a systematic analysis of acid-base status. The final step in the assessment of an acid-base disorder is to calculate the anion gap. A value greater than 20 mmol/L it is a definitive indication of the metabolic acidosis produced by some acid with an accompanying anion other than Cl- or HCO3-, for example, the production of formic acid from ingested ethanol causes a metabolic acidosis. Although an anion gap is expected only in metabolic acidosis, it should always be calculated because of the possibility of multiple coexisting acid-base disorders.

acid-base disorder is accompanied by a secondary one. In other words, that there is a mixed acid-base disorder. Note that the equations used for this analysis have been developed empirically by analysis of blood gas data from many patients. Nevertheless, these guidelines should not be regarded as absolute, and care should be taken to be sure that the diagnosis of the blood gas disorder is consistent with the history and physical observations for the patient.

The terminology used to describe acid-base disturbances can sometimes be confusing. It is best to reserve the terms acidosis and alkalosis for primary pathologic disturbances and not for physiologically appropriate compensatory mechanisms. Consider, for example, a patient with diabetic ketoacidosis who has a bicarbonate level of 14 mmol/L and the expected drop in Pco2 of 1.25 mm Hg for each 1 mmol/L of bicarbonate below 24 mmol/L (Pco2 = 28 mm Hg). This patient should be described as having a metabolic acidosis with respiratory compensation. From this perspective, it is not appropriate to refer to the respiratory response as a ''compensatory respiratory alkalosis'' because a normal physiologic response rather than a pathologic process produces it. On the other hand, patients often have a second pathologic process that produces what can be identified as an inappropriate compensation. Using the preceding example, if the patient had emphysema in addition to his or her diabetic ketoacidosis, the bicarbonate concentration of 14 mmol/L might be accompanied by a PCO2 of 38 mm Hg because the ventilatory defect prevents the expected decrease in PCO2 in response to the metabolic acidosis. Thus, the patient would be described as having both a metabolic and a respiratory acidosis. Despite the fact that the PCO2 of 38 is not significantly different from normal, it is much higher than would be expected in the presence of the metabolic acidosis.

The most difficult discrimination is often the etiology of a metabolic acidosis, because it can result from excessive acid intake or production or from excessive HCO3— loss. In these cases, an abnormal anion gap can point to the presence of excessive intake or production of an acid with accompanying anion as described in step 4 (Fig. 9). Although metabolic alkalosis is a less common disorder, its correction often is more dependent on restoring normal ECF volume and Cl— than on the acid loss or base excess itself.

Suggested Readings

Alpern RJ. Renal acidification mechanisms. In Brenner MB, ed. Brenner & Rectors the kidney, 6th ed. Philadelphia: WB Saunders, 2000, pp 455-519.

Andreoli TE, Cecil RL, Carpenter CCJ, Griggs RC, Loscalzo J. Cecil essentials of medicine, 5th ed. Philadelphia: WB Saunders, 2001, pp 245-252.

Halperin ML, Kamel KS, Ethier JM, Stinebaugh BJ, Jungas RL. Biochemistry and physiology of ammonium excretion. In Seldin DW, Giebisch G, eds. The kidney: Physiology and pathophysiology, Vol 2, 2nd ed. New York: Raven Press, 1992, pp 2645-2680.

Hamm L, Alpern RJ. Cellular mechanisms of renal tubular acidification. In Seldin DW, Giebisch G, eds. The kidney: Physiology and pathophysiology, Vol 2, 2nd ed. New York: Raven Press, 1992, pp 2581-2626.

Rose BD, Post TW. Clinical physiology of acid-base and electrolyte disorders, 5th ed. New York: McGraw-Hill, 2001, pp 647-695.

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