Introduction

  • Sodium bicarbonate was previously recommended for hyperkalemia treatment and was once considered a first-line agent for transcellular shift.
  • Studies evaluating the beneficial effects of sodium bicarbonate used an isotonic infusion, commonly ~150 mEq/1000 mL.
  • Hypertonic sodium bicarbonate (an "amp of bicarb") has an osmolality of ~2000 mOsm, about 7× higher than plasma.
  • There is controversy as to whether hypertonic sodium bicarbonate is beneficial for the acute treatment of hyperkalemia, owing to modifications in its mechanism of action.

Clinical Detail

Pharmacology — Sodium Bicarbonate

ParameterDetail
Dose
  • 0.5–1 mEq/kg IV bolus
  • 50–250 mEq/hr infusion
Formulations & administration
  • Hypertonic 8.4% (50 mEq/50 mL): slow IV push over 3–5 minutes
  • Isotonic 1.4% (150 mEq/L): 150–500 mL/hr over 2–6 hours
PK/PD
  • Onset (IV): 0.5–4 hours
  • Duration (IV): 4–6 hours
  • Excretion: urine (<1%)
Adverse effects
  • Hypocalcemia
  • Injection-site extravasation
  • Intracellular acidosis (without adequate ventilation)
  • Hypernatremia
  • Hyperosmolality
  • Shift in oxygen release by hemoglobin
CompatibilityIncompatible with epinephrine, calcium chloride, and calcium gluconate.

Proposed Mechanisms of Action

MechanismDescription
Transcellular shiftIndirect movement of potassium into cells via H+/K+ exchange and HCO3−/K+ cotransport.
Renal excretionK+ channels in the distal nephron are down-regulated by acidosis and up-regulated by alkalosis. Sodium bicarbonate (an alkalinizing agent) → K+ channel up-regulation → increased excretion of K+.
DilutionVolume expansion leads to less K+ per liter.

Evidence

Overview of Evidence

Author, yearDesign / sample sizeIntervention & comparisonOutcome
Ngugi, 1997Case series
n=10
  • Insulin 10 units + glucose 25 g
  • 8.4% SB 50 mL over 15 min
  • Salmeterol 0.5 mg IV
  • Combination of each
  • SB led to an average drop in K+ of 0.5 mEq/L at 30 minutes
  • Combination therapy with insulin/dextrose + salmeterol was more effective than SB alone
Kim, 1996Observational
n=12
  • 8.4% SB 120 mEq/L over 1 hr
  • Insulin drip 0.5 unit/kg/min over 1 hr
  • SB ↑ serum bicarbonate but no change in serum K+ (6.4 → 6.3 mEq/L)
  • Insulin drip ↓ serum K+ (6.3 → 5.7 mEq/L)
  • Insulin drip + SB ↓ serum K+ (6.2 → 5.2 mEq/L)
  • No change in K+ at hour 1 or 2
Blumberg, 1992Observational
n=12		8.4% SB (240 mEq/hr) over 1 hr, then 1.4% SB (30 mEq/hr) over 5 hrs↓ in serum K+ by 0.6 and 0.74 mEq/L at hours 4 and 6, respectively; approximately half of the reduction was calculated to be due to ECF volume expansion.
Gutierrez, 1991Observational
n=18
  • 1.4% SB in water (1 mEq/kg) over 2 hrs
  • 8.4% SB (1 mEq/kg) over 5 min
Peak T-waves on ECG (7 patients) disappeared after 1 hour in only 1 patient; isotonic SB ↑ bicarbonate by 3 mEq/L and ↓ K+ by 0.35 mEq/L at 180 min.
Blumberg, 1988Observational
n=10
  • 8.4% SB drip over 1 hr
  • 1.4% SB drip over 1 hr
  • Epinephrine drip 0.05 mcg/kg/min over 1 hr
  • Insulin drip 0.5 unit/kg/min over 1 hr
Hypertonic SB ↑ bicarbonate and osmolality slightly, with no change in K+; hypertonic and isotonic IV SB ↑ plasma bicarbonate and pH but had no impact on K+ (5.66 vs 5.83 mEq/L, before vs after).
Fraley, 1977Observational
n=14
  • SB 89–134 mEq/1000 mL D5W over 4–6 hours
  • D5W 1000 mL over 4–6 hours
In the SB-infusion group, serum K+ ↓ by ~0.15 mEq/L for every 1 mEq/L ↑ in bicarbonate; D5W was not effective in reducing potassium levels.
Schwarz, 1959Case series
N=4		5% SB drip over 2–6 hoursResolution of EKG abnormalities in all patients; 2/4 died within 24 hours.

Studies are small, older, and largely conducted in end-stage renal disease; interventions describe each study's protocol as reported in the source handout, not a dosing recommendation.

Conclusions

  • Sodium bicarbonate was historically considered a first-line agent for the transcellular shift of potassium, but its role in the acute treatment of hyperkalemia is now controversial.
  • The studies suggesting benefit generally used isotonic infusions (~150 mEq/1000 mL); the hypertonic "amp of bicarb" bolus carries a very high osmolality (~2000 mOsm, about 7× plasma).
  • Across the studies summarized above, bicarbonate alone produced little to no acute change in serum potassium, whereas insulin (with or without bicarbonate) lowered potassium; where a bicarbonate effect was seen, a substantial portion was attributed to extracellular-fluid volume expansion rather than transcellular shift.

References

  1. Sodium Bicarbonate. Micromedex [electronic version]. Greenwood Village, CO: Truven Health Analytics. Retrieved August 29, 2019. micromedexsolutions.com
  2. Gutierrez R, et al. Miner Electrolyte Metab. 1991;17(5):297-302. PMID: 1668124
  3. Fraley DS, et al. Kidney Int. 1977 Nov;12(5):354-60. PMID: 24132
  4. Blumberg A, et al. Am J Med. 1988 Oct;85(4):507-12. PMID: 3052050
  5. Blumberg A, et al. Kidney Int. 1992 Feb;41(2):369-74. PMID: 1552710
  6. Kim et al. Nephron. 1996;72(3):476-82. PMID: 8852501
  7. Ngugi NN, et al. East Afr Med J. 1997 Aug;74(8):503-9. PMID: 9487416
  8. Long B, et al. J Emerg Med. 2018 Aug;55(2):192-205. PMID: 29731287
Tags:hyperkalemia sodium bicarbonate potassium acidosis