SODIUM BICARBONATE 

1. BASIC PHYSIOLOGY & BUFFER SYSTEM

Bicarbonate Buffer System

CO2 +H2 O↔H2CO3 ↔H+ + HCO3−

• Governed by Henderson–Hasselbalch equation
• pH depends on:
• HCO₃⁻ (metabolic component)
• PaCO₂ (respiratory component)

Key principle:

• Giving bicarbonate → ↑ HCO₃⁻ → buffers H⁺ → forms CO₂ → requires adequate ventilation

If ventilation is poor → CO₂ retention → paradoxical intracellular acidosis

2. PREPARATIONS & FORMULATIONS

3. MECHANISM OF ACTION

Primary

• HCO₃⁻ binds H⁺ → carbonic acid → CO₂ + H₂O

Secondary ICU Effects

• ↑ pH → shifts potassium intracellular → ↓ serum K⁺
• ↑ sodium load → ↑ osmolality
• ↑ CO₂ production → ↑ ventilatory demand

4. INDICATIONS

STRONG INDICATIONS

1. Severe Metabolic Acidosis

• pH < 7.1 (some guidelines: < 7.0)

2. Hyperkalemia (Life-threatening)

• Mechanism:
• ↑ pH → K⁺ shifts intracellular

Adjunct (NOT first-line vs calcium/insulin)

3. Toxicology

4. Cardiac Arrest(American Heart Association)

• Not routine
• Consider in:
• Severe acidosis
• Hyperkalemia
• TCA overdose

5. Renal Failure with Acidosis

• When dialysis not immediately available

 NOT ROUTINELY INDICATED

• Mild/moderate metabolic acidosis
• Lactic acidosis (unless severe pH <7.1)
• Diabetic ketoacidosis (DKA) unless:
• pH < 6.9

Based on:American Diabetes Association

5. DOSE CALCULATION 

Bicarbonate Deficit Formula

HCO3 deficit=0.5×weight(kg)×(target−actualHCO3 )

Target HCO₃⁻:

• Usually 10–12 mEq/L (NOT full correction)

Practical ICU Approach

6.  ADVERSE EFFECTS 

1. Paradoxical CNS Acidosis

• CO₂ crosses BBB rapidly → worsens brain acidosis

2. Volume & Sodium Overload

3. Hypokalemia

4. Ionized Hypocalcemia—↓ contractility → ↓ BP

5. Metabolic Alkalosis

6. Increased CO₂ Load

Ventilator Strategy

• Must increase minute ventilation after bicarbonate

7. EVIDENCE & CONTROVERSIES 

BICAR-ICU Trial (2018)

• Severe metabolic acidosis (pH ≤7.2)
• Findings:
• No mortality benefit overall
• Benefit in AKI subgroup

 Supports selective use