Primary metabolic acid-base disorders

We will now turn our attention to the primary metabolic acid-base disorders.

When excess fixed acids are ingested or are produced metabolically (e.g., in lactic acidosis), pH falls, constituting acute metabolic acidosis. The drop in pH stimulates peripheral chemoreceptors, which, in turn, stimulate a rise in minute ventilation. The decline in arterial carbon dioxide tension mitigates the drop in pH produced by the metabolic acidosis.

The initial decline in bicarbonate is reflected in movement from point A to Point B along the arterial carbon dioxide tension isobar of 40 mmHg. With the resulting hyperventilation, arterial carbon dioxide tension declines to 20, returning arterial pH to normal, or near-normal, at 7.4, denoted by Point C. Point C indicates a compensated metabolic acidosis, and the low serum bicarbonate reflects the base deficit, denoted by the difference in bicarbonate concentrations between Points A and C.

When acidic body fluids are lost, e.g., loss of gastric acid with vomiting, or when excessive alkali is ingested, serum bicarbonate rises, resulting in acute metabolic alkalosis. The rise in pH results in decreased stimulation of peripheral chemoreceptors and, consequently, a decline in minute ventilation. The rise in arterial carbon dioxide tension mitigates the rise in pH produced by the metabolic alkalosis.

The initial increase in bicarbonate is reflected in movement from point A to Point B along the arterial carbon dioxide tension isobar of 40 mmHg. With the resulting hypoventilation, arterial carbon dioxide tension increases to 60, returning arterial pH to normal at 7.4, denoted as Point C. Point C indicates a compensated metabolic alkalosis, and the high serum bicarbonate reflects the base excess, denoted by the difference in bicarbonate concentrations between Points A and C.

In general, the magnitude of respiratory compensation for metabolic alkalosis is limited, and arterial carbon dioxide tension typically does not rise above 55 mmHg.

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