Bicarbonate Adjustment for Severe Metabolic Acidosis (CO2 16) on Hemodialysis
For a hemodialysis patient with severe metabolic acidosis (CO2 16 mEq/L), increase the dialysate bicarbonate concentration to 32-35 mEq/L and monitor pre- and post-dialysis CO2 levels to maintain pre-dialysis values ≥22 mEq/L while avoiding post-dialysis alkalosis (≤29 mEq/L). 1, 2
Understanding the Clinical Problem
A CO2 of 16 mEq/L represents severe metabolic acidosis that requires immediate intervention. This level is:
- Below the critical threshold of 22 mEq/L recommended by K/DOQI guidelines for all CKD patients, including those on dialysis 1
- Associated with significant morbidity including bone dissolution, protein catabolism, muscle wasting, and increased mortality risk 1, 3
- Particularly harmful as chronic metabolic acidosis alters calcium-PTH-vitamin D homeostasis, leading to progressive bone disease and fractures 1, 3
Dialysate Bicarbonate Prescription Strategy
Initial Adjustment
- Start with dialysate bicarbonate of 32-35 mEq/L for patients with pre-dialysis CO2 <22 mEq/L 2, 4, 5
- In a prospective study, 75% of patients achieving target acid-base control required dialysate bicarbonate concentrations of 32-34 mEq/L 2
- The standard "one-size-fits-all" approach of 35 mEq/L dialysate leaves many patients either acidotic before or alkalotic after dialysis 2
Target Goals
- Pre-dialysis CO2: 22-25 mEq/L (minimum ≥22 mEq/L) 1, 2, 5
- Post-dialysis CO2: ≤29 mEq/L to avoid metabolic alkalosis, which is independently associated with adverse outcomes 2, 4
Monitoring and Titration
- Measure pre- and post-dialysis CO2 levels at each session initially, then weekly once stable 2
- Adjust dialysate bicarbonate in 2-3 mEq/L increments based on response 2
- Nearly 100% of patients can achieve target ranges with individualized adjustment within the first month 2
Additional Factors Affecting Acid-Base Control
Key Determinants to Address
- Protein breakdown (increased protein nitrogen appearance) is independently associated with worse acidosis 6
- Dialysis adequacy (Kt/V) significantly impacts acid-base control—higher Kt/V reduces acidosis risk 6
- Calcium carbonate use as a phosphate binder provides additional alkali supplementation and reduces acidosis 6
Avoid Common Pitfalls
- Do not use citrate-containing alkali supplements in dialysis patients exposed to aluminum salts, as citrate increases aluminum absorption and worsens bone disease 1, 7
- Monitor for post-dialysis alkalosis, which can cause hemodynamic instability, increased hospitalizations, and mortality 2, 4
- Assess nutritional status in patients with persistently high bicarbonate (>25 mEq/L), as this typically indicates malnutrition and low endogenous acid production 8
Clinical Algorithm for Management
Confirm severe acidosis: Pre-dialysis CO2 = 16 mEq/L requires immediate intervention 1
Optimize dialysis adequacy: Ensure Kt/V >1.2 to enhance acid removal 6
Consider phosphate binder choice: Calcium carbonate provides additional alkali compared to non-calcium binders 6
Monitor response:
Titrate dialysate bicarbonate in 2-3 mEq/L increments until targets achieved 2
Reassess bone metabolism markers (calcium, phosphorus, PTH) as acidosis correction improves bone health 1, 3
Safety Considerations
- No increase in intradialytic adverse events has been observed with individualized bicarbonate adjustment to 32-34 mEq/L 2
- No clinically significant changes in calcium, phosphorus, PTH, sodium, or potassium occur with appropriate bicarbonate adjustment 2
- Avoid excessive correction that leads to post-dialysis alkalosis (>29 mEq/L), which is associated with adverse outcomes 2, 4