Clinical Note

Examples of Metabolic Acidosis

Because dangerous amounts of acid would rarely be ingested in normal foodstuffs, metabolic acidosis because of increased acid intake is usually observed only in poisoning. Typical causes of such poisoning also involve the simultaneous ingestion of an acid anion so that the anion gap increases. For example, among common acidic poisons, the metabolism of methyl alcohol results in formic acid, ethylene glycol in oxalic acid, paraldehyde in acetic acid, and aspirin in acetylsalicylic acid. However, ingestion of either ammonium chloride or hydrochloric acid will result in acidosis with a normal anion gap because the accompanying anion is Cl".

Increased metabolic production of acid is commonly observed in diabetic ketoacidosis, in which acetoacetic and ^-hydroxybutyric acid are produced. In severe illnesses with generalized poor tissue perfusion, toxic reactions, septicemia, or massive catabolism, high rates of lactic acid production may occur. In both diabetic ketoaci-dosis and lactic acidosis, the anion gap can be markedly elevated.

Chronic renal failure can also be associated with a buildup of the anions of weak acids that are not being excreted at high enough rates by the kidneys. Decreased glomerular filtration leads to a decreased excretion of titratable acidity, and the general decrease in renal mass decreases the ability of the kidney to form ammonium. Both of these effects compromise the ability of the kidney to generate HCO".

Loss of bicarbonate leading to metabolic acidosis can occur from either the gastrointestinal tract or the urine. The most common cause is the loss of HCO— and other ions in diarrhea, as occurs, for example, in inflammatory and infectious bowel diseases. Loss of HCO— by this route may also be iatrogenic because of the postoperative drainage of pancreatic juice or because of the routing of urine excretion through loops of bowel after surgical procedures in the lower urinary tract (ureterosigmoidostomy).

A less common cause of metabolic acidosis produced by excessive HCO— losses or decreased excretion of acid is renal tubular acidosis (RTA). RTA is due to a defect in the renal excretion of H+ or in the reabsorption of HCO— or both without a proportional impairment of GFR. In general, there are two forms of RTA: a proximal form characterized by impairment of proximal tubular HCO— reabsorption, resulting in bicarbonaturia (often the consequence of drugs that inhibit carbonic anhydrase), and a distal form characterized by an inability of the distal H+ transport mechanism to establish a normal gradient, resulting in the excretion of a relatively alkaline urine. Consequently, inadequate amounts of titratable acidity and NHj are excreted and positive acid balance develops. RTA is suspected when acidosis exists in the absence of an abnormal anion gap and there is no evidence of extrarenal alkali loss.

rise in HCO". However, respiratory compensation is limited by the fact the hypoventilation compromises the arterial PO2. Thus, the compensatory change in PCO2 is much less than with respiratory compensation for metabolic acidosis. With metabolic alkalosis, Pco2 rises by approximately 0.6 mm Hg for each 1 mmol/L rise in the HCO" concentration above the normal 24 mmol/L.

COMMON ACID-BASE DISTURBANCES: A SUMMARY

Figures 6 through 9 present a systematic approach to the analysis of common acid-base disturbances and their compensatory counterparts based on the information given in the preceding sections. Given a set of arterial blood gas determinations, the first step (Fig. 6) is to determine whether acidemia (pH < 7.37) or alkalemia (pH > 7.43) exists. However, even if the pH does not fall outside the normal range of 7.37-7.43, there may still be a mixture of acid-base disorders that fortuitously give a plasma pH in the normal range. For example, a metabolic alkalosis due to vomiting can be complicated by coexisting hypercapnia due to emphysema. For this reason, the other blood gas parameters (HCO3— and PCO2) should also be examined to determine if they fall in the normal ranges.

In step 2 of the analysis (Fig. 7), the Pco2 and HCO— values are examined, remembering that in respiratory

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