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General Considerations

A. Introduction

Metabolic acidosis is one of four cardinal acid–base disorders and is characterized by a decrease in the serum [HCO3] or [tCO2] below the value of 22 mEq/L. Because respiratory alkalosis can also cause a decline in plasma [HCO3] below normal, it is necessary to measure blood pH to distinguish between the two disorders. With metabolic acidosis, the pH is typically below the normal range of 7.35–7.45, while in respiratory alkalosis the pH is customarily above the normal range. Chronic respiratory alkalosis is the only acid base disorder for which the compensatory response can return the blood pH to normal (fully compensated). Therefore, an arterial blood gas is needed to make the precise acid base diagnosis. In addition, the clinical setting in which the disorder occurs is also helpful and is discussed below. Finally, other clinical tools (such as the serum anion gap [AG]) and simple calculations (comparison of the change in [HCO3] with the change in the AG from their respective normal values) can aid in making the appropriate acid–base diagnosis. Metabolic acidosis may occur because of an increase in endogenous organic acid production (such as lactate and ketoacids), a loss of bicarbonate (as with diarrhea), or an accumulation of endogenous acids because of inappropriately low excretion of net acid by the kidney (as in chronic kidney disease).

B. Neurorespiratory Response to Acidemia

The neurorespiratory control of ventilation is a critically important response to an acid load, and primary metabolic acidosis elicits predictable compensatory respiratory responses (secondary changes in Paco2). In general, a fall in systemic arterial pH is sensed by the chemoreceptors that stimulate ventilation and, therefore, reduce PaCO2. The fall in blood pH that would otherwise occur in uncompensated metabolic acidosis is blunted, therefore, but is not returned to the normal value, when metabolic acidosis is part of a simple (or single) acid base disturbance. Typically, the PaCO2 declines by an average of 1.25 mm Hg for each 1.0 mEq/L drop in HCO3 concentration. The appropriate value for the PaCO2 with physiologic compensation in steady-state metabolic acidosis can be estimated from the patient’s serum HCO3 concentration by application of the classical Winter equation:

PaCO2 = 1.5 (HCO3) + 8 ± 2 (mm Hg)


An easier but less accurate approach requires one to simply add the number 15 to the patient’s [HCO3] to quickly estimate the predicted (or compensatory) value for PaCO2 (valid in the pH range of 7.2–7.5). Approximately 12–24 hours is required to achieve full respiratory compensation for metabolic acidosis. However, since the decline in PaCO2 is limited by the accompanying ...

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