What does it mean to have low carbon dioxide (CO2) and low bicarbonate (HCO3) levels?

Low CO2 and Low HCO3: Metabolic Acidosis

Low CO2 (total carbon dioxide) and low bicarbonate (HCO3) on a basic metabolic panel indicate metabolic acidosis, a condition where the body has accumulated excess acid or lost bicarbonate, resulting in a primary reduction in serum bicarbonate below 22 mmol/L and typically associated with blood pH <7.35. 1, 2

Understanding the Measurements

• The "CO2" measured on a basic metabolic panel actually reflects total carbon dioxide content, which is predominantly bicarbonate (70-85%), with smaller amounts as dissolved CO2 and bound to hemoglobin 2
• Normal serum bicarbonate range is 22-26 mmol/L, and values below 22 mmol/L almost always indicate metabolic acidosis 2, 3
• When both CO2 and HCO3 are low together, this represents a primary metabolic problem (not respiratory), where the body has either lost bicarbonate or consumed it buffering excess acid 1, 4

Primary Mechanisms of Metabolic Acidosis

Metabolic acidosis develops through three main pathways:

• Increased acid production: Conditions like diabetic ketoacidosis, lactic acidosis from tissue hypoxia (shock, sepsis), or toxic ingestions generate excess acid that consumes bicarbonate during buffering 1, 5, 4
• Impaired renal acid excretion: Chronic kidney disease impairs the kidney's ability to excrete hydrogen ions and synthesize ammonia, leading to acid accumulation 2, 6
• Direct bicarbonate loss: Loss through the kidneys (renal tubular acidosis) or gastrointestinal tract (chronic diarrhea) directly depletes bicarbonate stores 1, 4

Diagnostic Algorithm

To determine the specific cause, calculate the anion gap:

• Normal anion gap (8-12 mEq/L): Indicates bicarbonate loss from kidneys or GI tract, or ingestion of certain chloride salts 3, 4
• Elevated anion gap (>12 mEq/L): Indicates presence of unmeasured acids such as lactate, ketones, uremic acids, or toxins 3, 4

Obtain arterial blood gas to assess:

• pH to confirm acidemia (pH <7.35) 1, 2
• PaCO2 to evaluate respiratory compensation (should be reduced as the body hyperventilates to blow off CO2) 1, 6
• Calculate expected compensation: PaCO2 should decrease by approximately 1.2 mmHg for every 1 mEq/L decrease in bicarbonate 3, 4

Clinical Significance and Consequences

Untreated metabolic acidosis causes multiple organ system dysfunction:

• Cardiovascular: Decreased cardiac contractility, arrhythmias, and impaired response to catecholamines 5
• Metabolic: Increased protein catabolism leading to muscle wasting, malnutrition, and negative nitrogen balance 2
• Skeletal: Bone demineralization and renal osteodystrophy as bone buffers chronic acid load 2
• Renal: Accelerated CKD progression when bicarbonate remains chronically low 2
• Pediatric: Growth retardation in children with chronic metabolic acidosis 2

Management Approach

Treatment must address the underlying cause while supporting acid-base balance:

Immediate Assessment

• Identify life-threatening causes requiring urgent intervention: diabetic ketoacidosis, septic shock, toxic ingestions, mesenteric ischemia 5, 6
• Monitor lactate levels as a marker of tissue hypoperfusion and shock severity 5
• Check serum potassium (often elevated in acidosis) and calcium (often decreased) 5

Treatment Thresholds Based on Bicarbonate Level

Bicarbonate ≥22 mmol/L: Monitor without pharmacological intervention 2

Bicarbonate 18-22 mmol/L:

• Consider oral alkali supplementation (sodium bicarbonate 0.5-1.0 mEq/kg/day divided into 2-3 doses) 2
• Monitor monthly initially, then every 3-4 months once stable 2
• In CKD patients, increase fruit and vegetable intake to provide natural alkali 2

Bicarbonate <18 mmol/L:

• Initiate pharmacological treatment with oral sodium bicarbonate immediately 2, 6
• Target maintenance of bicarbonate ≥22 mmol/L at all times 2
• Monitor blood pressure, serum potassium, and fluid status regularly as sodium bicarbonate can cause volume expansion 2

Specific Clinical Scenarios

Diabetic Ketoacidosis:

• Primary treatment is insulin therapy and fluid resuscitation, which corrects the underlying ketoacidosis 6
• Bicarbonate therapy is generally NOT indicated unless pH falls below 6.9-7.0 2, 6
• Monitor arterial or venous blood gases to assess treatment response 2

Lactic Acidosis from Shock:

• Focus on restoring tissue perfusion with fluid resuscitation and vasopressors 5, 6
• Sodium bicarbonate should NOT be used to treat metabolic acidosis from tissue hypoperfusion in sepsis 6
• Correct the underlying cause of shock rather than attempting to buffer the acid 6

Chronic Kidney Disease:

• Measure serum bicarbonate at least every 3 months for patients with GFR ≤30 ml/min per 1.73 m² 2
• Oral sodium bicarbonate supplementation slows CKD progression and prevents complications 2
• Avoid citrate-containing alkali in CKD patients exposed to aluminum salts as it increases aluminum absorption 2

Critical Pitfalls to Avoid

• Do not confuse with compensated respiratory acidosis: In chronic respiratory acidosis (elevated PaCO2), bicarbonate is HIGH as a compensatory mechanism, not low 1, 2
• Do not delay treatment of underlying cause: Bicarbonate supplementation alone is insufficient if the underlying acid-generating process continues 6, 4
• Do not over-correct: Target bicarbonate toward but not exceeding the normal range to avoid rebound alkalosis 2
• Do not ignore volume status: Sodium bicarbonate provides a significant sodium load; use cautiously in patients with heart failure, severe hypertension, or significant edema 2
• Do not assume normal anion gap is benign: Normal anion gap acidosis from diarrhea or renal tubular acidosis still requires treatment when bicarbonate falls below 18 mmol/L 2, 3