Primary metabolic acid-base disorders

Check out this article on primary metabolic acid-base disorders, and how to recognize them with a Davenport diagram.
Last update1st Dec 2020

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

Acute metabolic acidosis

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.

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Chronic (compensated) 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.

Figure 1. The Davenport diagram depicts the changes associated with chronic metabolic acidosis, including corrected arterial pH, decreased plasma bicarbonate (HCO3-), and decreased carbon dioxide tension (PaCO2).

Acute metabolic alkalosis

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.

Chronic (compensated) 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.

Figure 2. The Davenport diagram depicts the changes associated with chronic compensated metabolic alkalosis, including corrected arterial pH, increased plasma bicarbonate (HCO3-), and increased carbon dioxide tension (PaCO2).

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Recommended reading

  • Grippi, MA. 1995. “Gas exchange in the lung”. In: Lippincott's Pathophysiology Series: Pulmonary Pathophysiology. 1st edition. Philadelphia: Lippincott Williams & Wilkins. (Grippi 1995, 137–149)
  • Grippi, MA. 1995. “Clinical presentations: gas exchange and transport”. In: Lippincott's Pathophysiology Series: Pulmonary Pathophysiology. 1st edition. Philadelphia: Lippincott Williams & Wilkins. (Grippi 1995, 171–176)
  • Grippi, MA and Tino, G. 2015. “Pulmonary function testing”. In: Fishman's Pulmonary Diseases and Disorders, edited by MA, Grippi (editor-in-chief), JA, Elias, JA, Fishman, RM, Kotloff, AI, Pack, RM, Senior (editors). 5th edition. New York: McGraw-Hill Education. (Grippi and Tino 2015, 502–536)
  • Tino, G and Grippi, MA. 1995. “Gas transport to and from peripheral tissues”. In: Lippincott's Pathophysiology Series: Pulmonary Pathophysiology. 1st edition. Philadelphia: Lippincott Williams & Wilkins. (Tino and Grippi 1995, 151–170)
  • Wagner, PD. 2015. The physiologic basis of pulmonary gas exchange: implications for clinical interpretation of arterial blood gases. Eur Respir J45: 227–243. PMID: 25323225

About the author

Michael A. Grippi, MD
Michael is Vice Chairman in the Department of Medicine and Associate Professor of Medicine in the Pulmonary, Allergy, and Critical Care Division at the Perelman School of Medicine, University of Pennsylvania, USA.
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