10 pearls of Acid base

1. Normal pH, serum bicarbonate, and Pco2 levels do not necessarily exclude acid-base disorders. Final pH level is determined by the ratio of bicarbonate and Pco2. The terms “acidemia” and “alkalemia” represent only changes in pH, whereas the terms “acidosis” and “alkalosis” denote underlying pathological processes. Acidosis without acidemia and alkalosis without alkalemia can be seen. Remember to draw blood simultaneously for arterial blood gas measurement and for basic metabolic profile to ensure proper interpretation of acid-base disorders.

2. Always calculate the serum anion gap (AG); otherwise, acid-base disorders may go unrecognized. When calculating AG, pay attention to serum albumin values, which will influence AG significantly. For every 1 g/dL decline in serum albumin <4.4 g/dL, a 2.5 mEq/L reduction in AG occurs. In the case of increased AG, the ratio of AG and HCO3— should be calculated (Δ:Δ). The Δ:Δ<1 suggests mixed normal AG and high AG acidosis; Δ:Δ>2 suggests coexisting metabolic alkalosis. Increases in AG can be seen in nonacidotic states, such as metabolic alkalosis and respiratory alkalosis; however, increases in AG beyond 3 to 5 mEq/L are unusual.

3. Check for appropriate compensation to detect occult mixed acid-base disorders. Over- or undercompensation does not occur and is only indicative of another primary acid-base disorder. Any combination of acid-base disorder can occur, except for respiratory acidosis and respiratory alkalosis. In mixed acid-base disorders, therapeutic decisions should be based on the pH level.

4. Compensation formulas include:Expected compensation in metabolic acidosis:
Pco2 = 1.5 x HCO3— + 8 ±2
Expected compensation in metabolic alkalosis:
Pco2 = 0.6 x ΔHCO3—
Acute respiratory acidosis: ΔHCO3— = 0.1 x ΔPco2
Acute respiratory alkalosis: ΔHCO3— = 0.2 x ΔPco2
Chronic respiratory acidosis: ΔHCO3— = 0.35 x ΔPco2
Chronic respiratory alkalosis: ΔHCO3— = 0.4 x ΔPco2

Since you have to remember 4 formulas for expected compensatory changes in respiratory disorders, “1-4’’ can be used for quick recall.

5. The urinary AG (UAG) can be useful to differentiate between gastrointestinal (GI) and renal causes of a hyperchloremic metabolic acidosis. A negative UAG suggests GI loss of bicarbonate (eg, diarrhea); a positive UAG suggests impaired renal distal acidification (eg, distal renal tubular acidosis). UAG is not useful in volume depletion with urinary sodium <25 mEq/L.

6. In early stages of chronic kidney disease (glomerular filtration rate [GFR] <40 mL/min), normal AG metabolic acidosis can become evident, and as the disease progresses (GFR <20 mL/min), high AG metabolic acidosis can be seen. Serum bicarbonate <10 mEq/L and AG >20 mEq/L are unusual in renal failure and may be indicative of coexistent pathological processes, such as ketoacidosis or lactic acidosis.

7. Lactic acidosis that exceeds 4 to 5 mmol/L in a patient with acidosis is considered significant. The lactate level can exceed 12 mmol/L during grand mal seizures. Drug-induced lactic acidosis has been seen with metformin, isoniazid, and some antiretroviral agents.

8. In adults, salicylate overdose results in mixed metabolic acidosis and respiratory alkalosis; in children, only metabolic acidosis is seen.

9. Diabetic ketoacidosis, alcoholic ketoacidosis, lactic acidosis, and chronic renal failure—but not acute renal failure—are much more common causes of serum osmolal gap increases than are ethylene glycol or methanol intoxications. Serum osmolal gap can be seen without metabolic acidosis, for example, with isopropyl alcohol or with mannitol.

10. Serum osmolal gap of ≥25 mOsm/kg, in the absence of evident causes, strongly suggests methanol or ethylene glycol intoxication. Prophylactic therapy either with fomepizole or with ethanol can be initiated to prevent the formation of toxic metabolites while laboratory test results are pending. Once parent compounds are metabolized, the osmolal gap will disappear, but an increased AG will remain; hence, a normal osmolal gap does not necessarily exclude ethylene glycol or methanol toxicity.