What does a serum carbon dioxide (CO₂) level below 20 mmol/L indicate?

Serum CO₂ Below 20 mmol/L Indicates Metabolic Acidosis

A serum carbon dioxide level below 20 mmol/L indicates metabolic acidosis and requires immediate evaluation and treatment. 1

Understanding the Measurement

• The CO₂ measurement on a basic metabolic panel reflects total serum CO₂ content, which is predominantly bicarbonate (approximately 96% of the total), not arterial PCO₂. 1
• Normal serum CO₂ range is 22–26 mmol/L, though more recent evidence suggests tightening this to 23–30 mmol/L to avoid missing acid-base disorders. 1, 2
• Low serum bicarbonate concentrations (<22 mmol/L) almost always indicate metabolic acidosis, characterized by blood pH <7.35 and compensatory hyperventilation to eliminate CO₂. 1

Clinical Significance by Severity

Mild Metabolic Acidosis (18–22 mmol/L)

• Patients with bicarbonate 18–22 mmol/L can typically be managed as outpatients with oral alkali supplementation and dietary modifications. 1
• Consider oral sodium bicarbonate (0.5–1.0 mEq/kg/day divided into 2–3 doses) combined with increased fruit and vegetable intake. 1

Moderate to Severe Metabolic Acidosis (<18 mmol/L)

• Bicarbonate <18 mmol/L requires immediate pharmacological treatment with oral sodium bicarbonate, particularly in chronic kidney disease patients. 1
• In diabetic ketoacidosis, bicarbonate 15–18 mmol/L indicates mild DKA, while levels <15 mmol/L indicate moderate to severe DKA. 1
• Hospitalization is necessary for severe metabolic acidosis (<18 mmol/L), acute illness, catabolic states, symptomatic complications, or severe electrolyte disturbances. 1

Critical Acidosis (<10 mmol/L)

• In sepsis patients, TCO₂ ≤10 mmol/L is associated with 50% 28-day mortality and requires aggressive management. 3

Diagnostic Approach

Obtain arterial blood gas analysis to measure pH and PaCO₂ for complete acid-base assessment, especially in complex cases. 1

Calculate the Anion Gap

• Anion gap = Na⁺ − (HCO₃⁻ + Cl⁻), with normal values 10–12 mEq/L. 1
• Anion gap >12 mEq/L indicates accumulation of unmeasured anions (lactate, ketoacids, uremic toxins, ingested toxins). 1
• Normal anion gap suggests bicarbonate loss from diarrhea, renal tubular acidosis, or early chronic kidney disease. 1

Essential Laboratory Tests

• Serum electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻), plasma glucose, serum/urine ketones, BUN, and creatinine. 1
• In diabetic ketoacidosis, calculate effective serum osmolality: 2[Na (mEq/L)] + glucose (mg/dL)/18. 1

Management Principles

Chronic Kidney Disease (Most Common Cause)

• Maintain serum bicarbonate ≥22 mmol/L to prevent protein catabolism, bone disease, and CKD progression. 4, 1
• Monitor serum bicarbonate monthly in CKD stages 3–5, then every 3–4 months once stable. 4, 1
• Oral sodium bicarbonate 2–4 g/day (25–50 mEq/day) divided into 2–3 doses is first-line pharmacological treatment. 1
• Increasing fruit and vegetable intake provides additional benefits beyond bicarbonate supplementation alone, including reduced systolic blood pressure and potential weight loss. 1, 5

Diabetic Ketoacidosis

• Primary treatment is insulin therapy and fluid resuscitation, not bicarbonate. 1
• Administer isotonic saline 15–20 mL/kg/h during the first hour to restore intravascular volume. 1
• Start continuous IV regular insulin at 0.1 U/kg/h after confirming serum potassium >3.3 mEq/L. 1
• Bicarbonate therapy is NOT indicated unless pH falls below 6.9–7.0; when indicated, administer calculated amounts to bring pH up to 7.2, not to normalize it. 1
• Monitor venous pH and anion gap every 2–4 hours to assess treatment response. 1

Sepsis-Related Acidosis

• Focus treatment on restoring tissue perfusion with fluid resuscitation and vasopressors, not bicarbonate administration. 1
• Sodium bicarbonate should not be used to treat metabolic acidosis arising from tissue hypoperfusion in sepsis. 1

Critical Monitoring Parameters

• Serum potassium must be monitored closely (every 2–4 hours during acute treatment), as alkalinization drives potassium intracellularly and can precipitate life-threatening hypokalemia. 1
• Monitor blood pressure, fluid status, and serum electrolytes regularly after initiating treatment. 1
• Resolution criteria for DKA: glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, and venous pH ≥7.3. 1

Common Pitfalls to Avoid

• Do not ignore values at the lower end of the "normal" range (18–20 mmol/L) reported by some laboratories; these patients may have clinically important "hidden" acid-base disorders. 2
• Avoid citrate-containing alkali in CKD patients exposed to aluminum salts (e.g., aluminum-containing phosphate binders), as they may increase aluminum absorption and worsen bone disease. 1
• Do not administer bicarbonate empirically in high-anion-gap metabolic acidosis without first measuring pH; routine bicarbonate is contraindicated in most cases. 1
• In CKD patients hospitalized for acute illness, do not continue dietary protein restriction, as the catabolic state requires increased protein intake (1.2–1.5 g/kg/day). 1

Prognostic Implications

• In sepsis, serum TCO₂ concentrations ≤20 mmol/l show an almost linear correlation with mortality, with 28-day mortality rates increasing from 18.3% (>20 mmol/L) to 50.0% (≤10 mmol/L). 3
• Untreated chronic metabolic acidosis leads to increased protein catabolism and muscle wasting, bone demineralization, accelerated CKD progression, and growth retardation in children. 1