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Recognising mixed acid–base disorders

Worked examples showing mixed disorders despite normal pH, respiratory acidosis at a normal PaCO₂, and opposing metabolic effects.

Normal pH does not exclude a mixed disorder

Normal pH may reflect compensation or opposing primary disorders. Check SBE, measured metabolic contributors and the expected compensatory response. Use the history to establish the respiratory time course.

These synthetic teaching examples use the calculator’s equations. Each case opens with its full chemistry and interpretation.

Metabolic acidosis + respiratory alkalosis

pH 7.442PaCO₂ 18 mmHgHCO₃⁻ 12.0 mmol/LSBE −10.9 mEq/L
Metabolic acidosis + respiratory alkalosis

Expected PaCO₂: 24.0–28.0 mmHg. PaCO₂ is below expected compensation: additional respiratory alkalosis.

Lactate is 12 mmol/L and SBE is −10.9 mEq/L. PaCO₂ is below Winter’s range, indicating additional respiratory alkalosis. The pH is normal because the two disorders oppose each other.

Consider sepsis, salicylate exposure, or separate causes of metabolic acidosis and hyperventilation. The blood gas does not establish the underlying cause.

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Arterial sample; gas and chemistry from the same sampling time. Respiratory time course: Acute.

Metabolic acidosis + respiratory acidosis

pH 7.095PaCO₂ 40 mmHgHCO₃⁻ 12.0 mmol/LSBE −15.7 mEq/L
Metabolic acidosis + respiratory acidosis

Expected PaCO₂: 24.0–28.0 mmHg. PaCO₂ is above expected compensation: additional respiratory acidosis.

PaCO₂ is 40 mmHg. This is within the usual arterial interval but above the compensatory range for HCO₃⁻ 12.0 mmol/L. The result indicates additional respiratory acidosis.

Assess respiratory drive, airway obstruction, muscle weakness and ventilator settings where relevant. Check the clinical course for a recent change in ventilation.

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Arterial sample; gas and chemistry from the same sampling time. Respiratory time course: Acute.

Chronic respiratory acidosis — expected compensation

pH 7.366PaCO₂ 50 mmHgHCO₃⁻ 28.0 mmol/LSBE +2.9 mEq/L
Chronic respiratory acidosis

Chronic: 27.0–28.0 mmol/L. Within the expected chronic response.

HCO₃⁻ 28.0 mmol/L fits the chronic response to PaCO₂ 50 mmHg. Raised SBE alone does not establish a separate metabolic alkalosis.

Confirm chronic CO₂ retention from the history and a previous stable gas. If the time course is unknown, compare the acute and chronic compensation ranges.

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Arterial sample; gas and chemistry from the same sampling time. Respiratory time course: Chronic.

Raised lactate and low albumin — normal SBE

pH 7.400PaCO₂ 40 mmHgHCO₃⁻ 24.2 mmol/LSBE −0.2 mEq/L
Opposing metabolic effects; net SBE within the selected range

Lactate 5 mmol/L and chloride 110 mmol/L relative to sodium 140 mmol/L have acidifying effects. Albumin 20 g/L has an alkalinising effect. SBE remains within range.

Low albumin partly offsets the measured acidifying effects. It does not explain the entire balance; review the residual charge and contribution charts. Opposing contributions do not necessarily establish separate primary disorders.

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Arterial sample; gas and chemistry from the same sampling time. Respiratory time course: Acute.

Borderline compensation and suspected metabolic alkalosis

Compensation ranges are approximate. Before assigning another disorder to a borderline result, check sample timing, units, previous gases and treatment changes.

A raised delta ratio can suggest additional metabolic alkalosis. The selected anion-gap baseline and pre-existing chronic CO₂ retention affect this inference. It is not diagnostic on its own.

Case: metabolic acidosis + respiratory alkalosis + suspected metabolic alkalosis

Compensation rules and borderline results

Further reading

Adult blood gases at 37°C. Use and limitations.

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