Sodium bicarbonate administration should also be effective in lowering serum K+ levels. This happens when it directly decreases H+ concentration in the extracellular fluid compartment. High extracellular Na+ concentration leads to its increased cellular uptake and this creates an electric gradient that forces K+ out of the cell.
However, several studies using bicarbonate as monotherapy in hemodialysis patients failed to show a significant reduction in K+ concentration. In a small series of academic patients, bicarbonate therapy potentiated the potassium-lowering effect of insulin.
Based on this evidence, sodium bicarbonate is not effective for the treatment of acute hyperkalemia but it can be useful in a subset of patients with significant metabolic acidosis.

Sodium Bicarbonate
- Mechanism of Action:
- Indirect movement of potassium into cells via an H+/K+ exchange and HCO3-/K+ cotransport.
- K+ channels in the distal nephron are down-regulated by acidosis and up-regulated by alkalosis
- Sodium bicarbonate —> Alkalization agent —> K+ Channel upregulation –>↑ Excretion of K+
- Volume expansion leads to less K+ per liter
- Dose: Intravenous, NaHCO3, 50-100mEq or infusion at 150-300 ml/hr
- Hypertonic 8.4 % (50mEq/50 ml) Slow IV push over 3-5 minutes
- Isotonic Infusion 1.4% (150 mEq/L): 150-500 ml/hr x 2-6 hours
- Pharmacokinetics:
- Onset of Action: 15-30 mins
- Duration of Effect: 1-2 hours
- Contraindications: Patients with heart failure, hypernatremia, patient with respiratory insufficiency due to bicarbonate
- Adverse Effects: Hypocalcemia, injection site extravasation, intracellular acidosis, hypernatremia, hyperosmosis, shift O2 release by hemoglobin
- Pearls: Potentiates potassium-lowering effect of insulin; not beneficial for patients with acute hyperkalemia but useful for those with significant metabolic acidosis
- Incompatible with Epinephrine, calcium chloride, and calcium gluconate
Overview of Evidence for Sodium Bicarbonate for Hyperkalemia in the Emergency Department
Author, Year | Design or Sample Size | Intervention & Comparison | Outcome |
Ngugi, 1997 | Case Seriesn=10 | Insulin- 10 unit + glucose 25g8.4% SB- 50 ml over 15 minsSalmeterol- 0.5 mg IVCombination of each | SB led to an average ↓ in K+ by 0.5 mEq/L drop at 30 minutes Combination therapy with insulin/dextrose + Salmeterol was more effective than those with SB |
Kim, 1996 | Observationaln=12 | 8.4% SB-120 mEq/L x 1 hr Insulin drip- 0.5 unit/kg/min x 1 hr | SB led to ↑ of serum bicarbonate but no change in serum K+ (6.4 mEq/L to 6.3 mEq/L) Insulin drip led to ↓ of serum K+ (6.3 mEq/L to 5.7 mEq/L) Combination of insulin drip + SB led to ↓ in serum K+(6.2 mEq/L to 5.2 mEq/L) |
Blumberg, 1992 | Observationaln=12 | 8.4% SB (240 mEq/hr) x 1hr then with1.4% SB (30 mEq /hr) x 5 hrs | No change in K+ at hour 1 or 2 ↓ in serum K+ by 0.6 and 0.74 mEq/L at hours 4 and 6 respectively, of which approximately half was calculated to be due to ECF volume expansion Peak T-waves in the ECG of 7 patients disappeared after one hour only in one patient |
Gutierrez, 1991 | Observationaln=18 | 1.4% SB in H2O (1mEq/kg) over 2 hrs 8.4% SB(1mEq/kg) over 5 mins | Isotonic SB led to ↑ in bicarbonate by 3 mEq/L and ↓ K+ by 0.35 mEq/L at 180 min Hypertonic SB led to slight ↑ in bicarbonate and Osmolality and no change in K+ levels |
Blumberg, 1988 | Observationaln=10 | 8.4% SB drip x 1 hr 1.4% SB drip x 1 hr Epinephrine drip 0.05mcg/kg/min x 1 hr Insulin drip 0.5 unit/kg/min x 1 hr | Hypertonic and isotonic IV SB = ↑plasma bicarbonate and pH, but no impact on K+(5.66 versus 5.83 mEq/L) before vs after |
Fraley, 1977 | Observationaln=14 | SB 89-134 mEq/1000ml D5W over4-6 hoursD5W 1000ml over 4-6 hours | In SB infusion group, serum K+ ↓ by about 0.15 mEq/L for every 1 mEq/L ↑ in bicarbonate D5W was not effective in reducing potassium levels |
Schwarz, 1959 | Case SeriesN=4 | 5% SB drip over 2-6 hours | Resolution of EKG abnormalities in all patients; 2/4 died within 24 hours |