What does a low bicarbonate (HCO3) level indicate on an arterial blood gas (ABG)?

Low HCO3 on ABG: Clinical Interpretation

A low bicarbonate (HCO3) level on arterial blood gas indicates metabolic acidosis, characterized by primary reduction in serum bicarbonate below 22 mmol/L with blood pH typically less than 7.35, requiring immediate investigation of the underlying cause and assessment of compensatory respiratory response. 1, 2

Understanding the Measurement

• Normal serum bicarbonate range is 22-26 mmol/L, and values below this threshold almost always indicate metabolic acidosis 1, 2
• Low serum bicarbonate concentrations represent a primary metabolic disturbance where the body has lost buffering capacity against acids 1
• The body attempts to compensate by increasing ventilation to eliminate CO2, with an expected decrease in PaCO2 of approximately 1 mmHg for every 1 mmol/L fall in serum HCO3 2

Diagnostic Algorithm

Step 1: Confirm Metabolic Acidosis

• Check pH and PaCO2 simultaneously - if pH is <7.35 with normal or low PaCO2, this confirms metabolic acidosis rather than respiratory compensation 3
• If pH is <7.35 with PaCO2 >6.0 kPa (45 mmHg), this indicates respiratory acidosis with possible mixed disorder 3

Step 2: Calculate Anion Gap

• Calculate anion gap as [Na+] - ([HCO3-] + [Cl-]) to categorize the acidosis into high anion gap or normal (hyperchloremic) anion gap metabolic acidosis 4
• High anion gap metabolic acidosis typically results from overproduction of organic acids (ketoacids, lactic acid) 2
• Normal anion gap metabolic acidosis reflects bicarbonate wasting or impaired renal acidification 2

Step 3: Identify Severity Thresholds

Critical severity markers:

• HCO3 <18 mmol/L requires pharmacological treatment with sodium bicarbonate, particularly in chronic kidney disease patients 1
• HCO3 15-18 mmol/L indicates mild diabetic ketoacidosis 1
• HCO3 <15 mmol/L indicates moderate to severe diabetic ketoacidosis 1
• Base deficit is an independent predictor of mortality in traumatic hemorrhagic shock 5

Clinical Context Matters

Acute vs. Chronic Metabolic Acidosis

Acute metabolic acidosis (minutes to days):

• Most frequently results from overproduction of organic acids such as lactic acid in shock states 5, 2
• Adverse effects include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, and predisposition to arrhythmias 2
• In septic shock, exhibits complex metabolic acidosis with contributions from lactic acidosis, hyperchloremic acidosis, and increased strong ion gap 5

Chronic metabolic acidosis (weeks to years):

• Often reflects bicarbonate wasting and/or impaired renal acidification, particularly in chronic kidney disease 2
• Main adverse effects include increased muscle degradation, abnormal bone metabolism, protein catabolism leading to muscle wasting, and bone demineralization 1, 2
• In CKD patients, serum bicarbonate should be monitored monthly and maintained at or above 22 mmol/L 1

Special Populations

Patients at risk of hypercapnic respiratory failure:

• If pH <7.35 with PCO2 >6.0 kPa and low HCO3, this represents mixed respiratory and metabolic acidosis requiring immediate senior review and consideration of NIV or invasive ventilation 3
• Target oxygen saturation of 88-92% in COPD patients, severe obesity, cystic fibrosis, or neuromuscular disease to avoid worsening hypercapnia 3

Critically ill patients:

• Serial measurements of lactate, base deficit, and pH provide valuable information about shock severity and response to treatment 5
• Elevated lactate levels (>2 mmol/L) indicate tissue hypoxia and correlate with mortality 5

Common Pitfalls to Avoid

• Do not assume normal oxygen saturation excludes metabolic acidosis - pulse oximetry will be normal in patients with normal PO2 but abnormal pH or PCO2 3
• Do not confuse compensatory bicarbonate retention with primary metabolic alkalosis - in chronic respiratory acidosis, kidneys retain bicarbonate as compensation, resulting in high bicarbonate levels but as a compensatory mechanism 1
• Do not draw ABG during apneic phase in OSA patients - this can show severe metabolic acidosis that reverses once the patient awakens, leading to clinical decision errors 6
• Do not overlook mixed acid-base disorders - when the anion gap is compared with changes in bicarbonate concentration, other occult acid-base disorders can be identified 4

Management Principles

For acute metabolic acidosis:

• Focus on treating the underlying cause rather than administering bicarbonate therapy 1
• In diabetic ketoacidosis, bicarbonate therapy is generally not indicated unless pH falls below 6.9-7.0 1
• In septic shock, sodium bicarbonate should not be used to treat metabolic acidosis from tissue hypoperfusion - instead restore tissue perfusion with fluid resuscitation and vasopressors 1

For chronic metabolic acidosis:

• Initiate oral sodium bicarbonate when serum bicarbonate falls below 22 mmol/L, with aggressive treatment required when levels drop below 18 mmol/L 1
• Typical dosing is 0.5-1.0 mEq/kg/day divided into 2-3 doses 1
• Monitor serum bicarbonate monthly initially, then at least every 4 months once stable, along with blood pressure, serum potassium, and fluid status 1