Test Description

What is Total CO2?

The "CO2" reported on a basic or comprehensive metabolic panel (BMP/CMP) is actually total CO2 content, which includes:

  • Bicarbonate (HCO3⁻): ~95% of total CO2
  • Dissolved CO2: ~5% (includes carbonic acid and dissolved CO2 gas)

For practical purposes, serum CO2 is essentially equivalent to bicarbonate and reflects the metabolic component of acid-base status.

CO2 vs ABG Bicarbonate

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Feature Serum CO2 (BMP/CMP) ABG Bicarbonate
Sample Venous blood Arterial blood
Measurement Directly measured total CO2 Calculated from pH and pCO2
Values 1-2 mEq/L higher than ABG HCO3 Slightly lower
Use Screening, monitoring Definitive acid-base analysis
Clinical Correlation: Serum CO2 is a useful screening tool, but for complete acid-base assessment, an arterial blood gas is needed to determine pH, pCO2, and differentiate between metabolic and respiratory disorders.
Quick Reference
  • Normal Range: 22-29 mEq/L (or mmol/L)
  • Low CO2: <22 mEq/L (metabolic acidosis or respiratory alkalosis compensation)
  • High CO2: >29 mEq/L (metabolic alkalosis or respiratory acidosis compensation)
  • Primary Use: Screen for acid-base disturbances on basic metabolic panel
  • Sample Type: Serum or plasma (various tube types)
  • Key Point: CO2 on BMP/CMP is ~95% bicarbonate; use ABG for definitive acid-base analysis
Normal Ranges
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Age Group Normal CO2 (mEq/L) Notes
Adults 22-29 Standard reference range
Newborns 13-22 Lower due to physiologic acidosis
Infants 20-28 Approaching adult values
Children 20-28 Similar to adults
Critical Values:
  • CO2 <12 mEq/L: Severe metabolic acidosis - immediate evaluation needed
  • CO2 >40 mEq/L: Severe metabolic alkalosis - risk of arrhythmias
Clinical Significance

Low CO2 (<22 mEq/L)

Low serum CO2 indicates either metabolic acidosis (primary) or compensation for respiratory alkalosis.

Metabolic Acidosis - High Anion Gap (MUDPILES):

  • Methanol
  • Uremia (renal failure)
  • Diabetic ketoacidosis (DKA)
  • Propylene glycol
  • Isoniazid, Iron
  • Lactic acidosis
  • Ethylene glycol
  • Salicylates

Metabolic Acidosis - Normal Anion Gap (HARDUPS):

  • Hyperalimentation
  • Acetazolamide, Addison's disease
  • Renal tubular acidosis
  • Diarrhea
  • Ureteral diversion
  • Pancreatic fistula
  • Saline infusion (dilutional)

Respiratory Alkalosis with Compensation:

  • Hyperventilation (anxiety, pain, fever)
  • Sepsis (early)
  • Pulmonary embolism
  • High altitude
  • CNS disorders

High CO2 (>29 mEq/L)

High serum CO2 indicates either metabolic alkalosis (primary) or compensation for respiratory acidosis.

Metabolic Alkalosis:

  • Volume contraction: Vomiting, NG suction, diuretic use
  • Hypokalemia: Causes renal bicarbonate retention
  • Hyperaldosteronism: Primary or secondary
  • Alkali ingestion: Antacids, bicarbonate administration
  • Post-hypercapnic alkalosis: After correcting chronic respiratory acidosis
  • Bartter/Gitelman syndrome: Rare genetic disorders

Respiratory Acidosis with Compensation:

  • COPD (chronic)
  • Obesity hypoventilation syndrome
  • Neuromuscular disease
  • Severe asthma (late/severe)
The Anion Gap: Calculate anion gap (Na - Cl - CO2) to help differentiate causes of metabolic acidosis. Normal anion gap is 8-12 mEq/L. High anion gap (>12) indicates unmeasured acids (ketones, lactate, toxins).
Interpretation Guidelines

Approach to Abnormal CO2

Step 1: Is the patient symptomatic?

  • Metabolic acidosis: Kussmaul breathing, confusion, fatigue
  • Metabolic alkalosis: Muscle cramps, tetany, arrhythmias

Step 2: Calculate the anion gap

Anion Gap = Na⁺ - (Cl⁻ + CO2)

  • Normal: 8-12 mEq/L
  • Elevated (>12): Suggests addition of unmeasured acid

Step 3: Get an ABG if needed for complete picture

  • Determines if acidemia or alkalemia (pH)
  • Identifies respiratory component (pCO2)
  • Allows calculation of expected compensation

Expected Compensation

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Primary Disorder Expected Compensation
Metabolic Acidosis pCO2 = 1.5 × HCO3 + 8 (±2) (Winter's formula)
Metabolic Alkalosis pCO2 increases 0.7 mmHg per 1 mEq/L rise in HCO3
Acute Respiratory Acidosis HCO3 increases 1 mEq/L per 10 mmHg rise in pCO2
Chronic Respiratory Acidosis HCO3 increases 3.5 mEq/L per 10 mmHg rise in pCO2
Interfering Factors

Pre-analytical Errors

  • Exposure to air: CO2 escapes from uncapped samples, causing falsely low values
  • Delayed analysis: Cellular metabolism can alter CO2 levels
  • Tourniquet time: Prolonged stasis can cause mild lactate accumulation

Medications Affecting CO2

  • Decrease CO2: Acetazolamide, aspirin (high dose), metformin, topiramate
  • Increase CO2: Thiazide/loop diuretics, corticosteroids, sodium bicarbonate, antacids

Analytical Interference

  • Hemolysis: May affect some analyzer methods
  • Lipemia: Can interfere with certain measurements
Clinical Pearls
The "vomiting" CO2: Persistent vomiting causes metabolic alkalosis (high CO2) due to loss of gastric HCl. The triad of high CO2, low chloride, and low potassium strongly suggests this etiology.
Low CO2 in DKA: A very low CO2 (<10 mEq/L) in a diabetic patient is DKA until proven otherwise. Check glucose, ketones, and get an ABG. The lower the CO2, the more severe the acidosis.
Contraction alkalosis: Diuretic use causes volume contraction and preferential chloride loss, leading to "contraction alkalosis." Correcting volume with normal saline often corrects the alkalosis.
COPD trap: A "normal" CO2 of 24 mEq/L in a known COPD patient with chronic hypercapnia may actually represent acute metabolic acidosis superimposed on chronic respiratory acidosis. Know your patient's baseline.
When to order ABG: Order an ABG when you need to know the pH (acidemia vs alkalemia), when CO2 is abnormal, when respiratory distress is present, or when you need to assess oxygenation. Serum CO2 alone cannot determine if a patient is acidemic or alkalemic.
Delta-delta ratio: In high anion gap metabolic acidosis, calculate: (Change in anion gap) ÷ (Change in HCO3). Ratio 1-2 = pure HAGMA. Ratio >2 = concurrent metabolic alkalosis. Ratio <1 = concurrent non-gap acidosis.
References
  1. Kratz, A., Ferraro, M., Sluss, P. M., & Lewandrowski, K. B. (2004). Laboratory reference values. New England Journal of Medicine, 351, 1548-1564.
  2. Berend, K., de Vries, A. P., & Gans, R. O. (2014). Physiological approach to assessment of acid-base disturbances. New England Journal of Medicine, 371(15), 1434-1445.
  3. Seifter, J. L. (2014). Integration of acid-base and electrolyte disorders. New England Journal of Medicine, 371(19), 1821-1831.
  4. Emmett, M., & Narins, R. G. (1977). Clinical use of the anion gap. Medicine, 56(1), 38-54.
  5. Narins, R. G., & Emmett, M. (1980). Simple and mixed acid-base disorders: a practical approach. Medicine, 59(3), 161-187.
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  • For Educational Purposes Only: This content is intended for educational reference and should not be used for clinical decision-making.
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The clinical content and references are curated and reviewed by myself; however, AI was used to assist in organizing, paraphrasing, and formatting the information presented.