2 Metabolic and Respiratory Acid–Base Disorders

A practical approach to ABGs

An ABG (arterial blood gas) provides values used to identify an acid–base pattern, not its cause. Interpret the results alongside the patient’s condition and investigate the underlying problem.

Typical adult reference ranges are pH $7.35$–$7.45$, PaCO₂ $35$–$45$ mm Hg, and HCO₃⁻ $22$–$26$ mEq/L. Local laboratory ranges may vary.

A useful interpretation sequence is:

1. Check pH. A pH below $7.35$ indicates acidemia; a pH above $7.45$ indicates alkalemia.

2. Identify the primary change. HCO₃⁻ points to a metabolic disorder, while PaCO₂ points to a respiratory disorder. In metabolic disorders, pH and HCO₃⁻ move in the same direction. In respiratory disorders, pH and PaCO₂ move in opposite directions.

3. Check compensation. The other system should respond in the expected direction and range. Compensation does not normally overshoot or fully normalize the pH. An unexpected response suggests a second primary disorder.

4. Use the clinical context. The ABG identifies the pattern, so evaluate the patient and look for the underlying cause.

Primary disorders and compensation

In a metabolic disorder, the primary change is in HCO₃⁻ and the respiratory system compensates. In a respiratory disorder, the primary change is in PaCO₂ and the kidneys compensate. The expected patterns are:

• Metabolic acidosis: HCO₃⁻ decreases; increased ventilation decreases PaCO₂.

• Metabolic alkalosis: HCO₃⁻ increases; decreased ventilation increases PaCO₂.

• Respiratory acidosis: PaCO₂ increases; the kidneys retain HCO₃⁻. Greater renal compensation develops over days.

• Respiratory alkalosis: PaCO₂ decreases; the kidneys excrete HCO₃⁻. Greater renal compensation develops over days.

For metabolic acidosis, estimate expected respiratory compensation with Winter’s formula:

The measured PaCO₂ should fall within the predicted range if the respiratory response is appropriate. A value outside that range suggests an additional respiratory disorder.

Causes and manifestations

Causes and symptoms can help guide evaluation, but symptoms vary with severity, speed of onset, and underlying illness. Treating the cause is more important than treating an isolated ABG number.

Metabolic disorders

Metabolic acidosis may result from increased acid production, such as lactic acidosis or ketoacidosis; reduced renal acid excretion; or bicarbonate loss, such as with diarrhea. Deep, rapid breathing may be a compensatory response. Severe acidemia can impair cardiovascular and neurologic function.

Metabolic alkalosis may result from acid loss through vomiting or gastric suction, diuretic use, or excess bicarbonate. Weakness, cramps, or other symptoms may occur, sometimes related to low potassium or volume depletion.

Respiratory disorders

Respiratory acidosis can result from inadequate ventilation, for example due to airway or lung disease, sedative or opioid effects, or neuromuscular weakness. Drowsiness, confusion, or headache may occur, particularly with acute or severe carbon dioxide retention.

Respiratory alkalosis can result from excessive ventilation associated with pain, fever, hypoxemia, pulmonary embolism, pregnancy, or sepsis. Lightheadedness and tingling may occur. Investigate the cause rather than assuming anxiety.

Worked ABG cases

Use the pH and primary change to identify the disorder, then compare the compensatory response with what is expected.

Diarrhea and acidemia

A patient with several days of severe diarrhea has pH $7.25$, PaCO₂ $27$ mm Hg, and HCO₃⁻ $12$ mEq/L. This is metabolic acidosis with appropriate respiratory compensation: the low pH and low HCO₃⁻ identify the primary metabolic process. Winter’s formula predicts:

The measured PaCO₂ of $27$ mm Hg is within the predicted range. Diarrheal bicarbonate loss is a common cause.

Vomiting

A patient with persistent vomiting has pH $7.50$, PaCO₂ $48$ mm Hg, and HCO₃⁻ $36$ mEq/L. This is metabolic alkalosis: the high pH and high HCO₃⁻ identify the primary metabolic process. The elevated PaCO₂ reflects compensatory hypoventilation. Vomiting can cause acid loss and volume depletion.

Hypoventilation after sedating medication

A patient who is difficult to awaken after taking sedating medication has pH $7.25$, PaCO₂ $60$ mm Hg, and HCO₃⁻ $26$ mEq/L. This is acute respiratory acidosis: the low pH and elevated PaCO₂ point to primary hypoventilation, while the near-normal HCO₃⁻ is consistent with little time for renal compensation. Prioritize airway, breathing, and circulation; support ventilation as needed and promptly assess and treat the cause, including possible medication toxicity.

Chronic lung disease

A patient with chronic obstructive pulmonary disease has a stable ABG with pH $7.34$, PaCO₂ $60$ mm Hg, and HCO₃⁻ $32$ mEq/L. This is chronic respiratory acidosis with renal compensation: the elevated PaCO₂ is primary, and increased HCO₃⁻ suggests renal retention over time. The pH remains slightly low, so the disorder is not fully compensated to normal.

Fever and rapid breathing

A patient with fever and rapid breathing has pH $7.50$, PaCO₂ $28$ mm Hg, and HCO₃⁻ $21$ mEq/L. This is respiratory alkalosis: the high pH and low PaCO₂ indicate excessive ventilation as the primary process. Rapid breathing should not automatically be treated as anxiety; assess for causes such as hypoxemia, infection, pain, or pulmonary embolism.

Checking for a mixed disorder

A patient with metabolic acidosis has HCO₃⁻ $12$ mEq/L and measured PaCO₂ $40$ mm Hg. Winter’s formula predicts PaCO₂ $26 \pm 2$ mm Hg, so $40$ mm Hg is not the expected compensatory response. It is higher than expected, suggesting an additional respiratory acidosis or inadequate ventilatory compensation.

Treatment priorities

Begin with the patient rather than the ABG number. Assess airway, breathing, circulation, mental status, oxygenation, and severity, and stabilize urgent threats.

Address the cause. Examples include restoring appropriate ventilation, treating the underlying lung or systemic illness, and correcting gastrointestinal or renal fluid and electrolyte losses. Repeat clinical assessment and blood gases as appropriate; unexpected compensation should prompt evaluation for a mixed disorder.

Avoid reflexive correction. Treatment decisions depend on the cause and the patient’s overall clinical state. Changing pH without addressing the underlying problem may be harmful.