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Lesson 8 of 11
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Sodium Bicarbonate

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, YearDesign or Sample SizeIntervention & ComparisonOutcome
Ngugi, 1997Case Seriesn=10Insulin- 10 unit + glucose 25g8.4% SB- 50 ml over 15 minsSalmeterol- 0.5 mg IVCombination of eachSB 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, 1996Observationaln=128.4% 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, 1992Observationaln=128.4% SB (240 mEq/hr) x 1hr then with1.4% SB (30 mEq /hr) x 5 hrsNo 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, 1991Observationaln=181.4% 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, 1988Observationaln=108.4% 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, 1977Observationaln=14SB 89-134 mEq/1000ml D5W over4-6 hoursD5W 1000ml over 4-6 hoursIn 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, 1959Case SeriesN=45% SB drip over 2-6 hoursResolution of EKG abnormalities in all patients; 2/4 died within 24 hours