Primary respiratory acid-base disorders

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

The primary acid-base disorders include respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Furthermore, each of these can exist as either acute or chronic conditions. Here we will discuss the primary respiratory acid-base disorders; later we will discuss the metabolic disorders.

Acute respiratory acidosis

Hypercapnia arising from alveolar hypoventilation leads to respiratory acidosis. Consider a Davenport diagram-based depiction of the changes associated with a rise in arterial carbon dioxide tension from 40 to 60 mmHg.

Starting at an arterial carbon dioxide tension of 40, serum bicarbonate of 24, and a pH of 7.4, an immediate rise in arterial carbon dioxide tension to 60 results in a pH drop to about 7.3 (Point A to Point B).

The resulting acid-base disorder is known as acute respiratory acidosis.

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

When arterial carbon dioxide tension is chronically elevated, renal compensation results in increased serum bicarbonate and incomplete correction of pH. As bicarbonate increases, movement along the arterial carbon dioxide tension isobar to Point C occurs. The elevation in bicarbonate from 24 to 38 mmol as a result of renal compensation constitutes a base excess of 14 mmol.

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The disorder is referred to as a compensated respiratory acidosis or chronic respiratory acidosis.

Figure 2. The Davenport diagram depicts the changes associated with chronic respiratory acidosis, including the incomplete correction of arterial pH, chronically increased plasma bicarbonate (HCO3-), and increased carbon dioxide tension (PaCO2).

Acute respiratory alkalosis

Hypocapnia arising from alveolar hyperventilation leads to respiratory alkalosis. Consider the changes associated with a decrease in arterial carbon dioxide tension from 40 to 20 mmHg.

Starting at an arterial carbon dioxide tension of 40, serum bicarbonate of 24, and pH of 7.4, an immediate decrease in arterial carbon dioxide tension to 20 results in a pH rise to about 7.6 (Point A to Point B).

The resulting acid-base disorder is known as acute respiratory alkalosis.

Figure 3. The Davenport diagram depicts the changes associated with acute respiratory alkalosis, including increased arterial pH, decreased plasma bicarbonate (HCO3-), and decreased carbon dioxide tension (PaCO2).

Chronic (compensated) respiratory alkalosis

When arterial carbon dioxide tension is chronically decreased, the kidneys compensate by excreting more bicarbonate, correcting the pH. The correction may be nearly complete. The decline in bicarbonate from 24 to 12 mmol as a result of renal compensation constitutes a base deficit of 12 mmol / L.

The disorder is referred to as a compensated respiratory alkalosis or chronic respiratory alkalosis.

Figure 4. The Davenport diagram depicts the changes associated with chronic respiratory alkalosis, including corrected arterial pH, chronically decreased plasma bicarbonate (HCO3-), and decreased 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
Vice Chairman, Department of Medicine | Pulmonary, Allergy, and Critical Care Division, Perelman School of Medicine, University of Pennsylvania, USA.
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