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/ 1000ml
Hypertonic sodium bicarbonate or “amp of bicarb” has an osmolality of 2000 mOsm, about 7x higher than plasma. There’s controversy as to whether hypertonic sodium bicarbonate is beneficial for the acute treatment of hyperkalemia due to modifications in mechanism of action.
Key Points
- Sodium bicarbonate was once considered a first-line agent for the transcellular shift of potassium in hyperkalemia.
- The studies showing benefit used ISOTONIC bicarbonate infusions (~150 mEq/L), not the hypertonic “amp of bicarb” (~2000 mOsm, about 7× plasma).
- There is controversy over whether hypertonic sodium bicarbonate actually lowers potassium acutely.
- Insulin/dextrose, beta-2 agonists (e.g., albuterol), and calcium remain the preferred acute agents for hyperkalemia.
Clinical Detail
| Parameter | Sodium Bicarbonate |
|---|---|
| Dose | 0.5–1 mEq/kg IV bolus 50–250 mEq/hr infusion |
| Administration | Hypertonic 8.4% (50 mEq/50 mL): slow IV push over 3–5 minutes Isotonic infusion 1.4% (150 mEq/L): 150–500 mL/hr x 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 Hyperosmosis Shift of O2 release by hemoglobin |
| Compatibility | Incompatible with epinephrine, calcium chloride, calcium gluconate |
Proposed Mechanisms of Action
| Proposed Mechanism | Description |
|---|---|
| Transcellular shift | Indirect movement of potassium into cells via an H+/K+ exchange and HCO3−/K+ cotransport. |
| Renal excretion | K+ channels in the distal nephron are down-regulated by acidosis and up-regulated by alkalosis. Sodium bicarbonate (alkalinization agent) → K+ channel upregulation → ↑ excretion of K+. |
| Dilution | Volume expansion leads to less K+ per liter. |
Evidence
| Author, Year | Design / Sample Size | Intervention & Comparison | Outcome |
|---|---|---|---|
| Ngugi, 1997 | Case series n=10 | Insulin 10 units + glucose 25 g 8.4% SB 50 mL over 15 mins Salmeterol 0.5 mg IV Combination of each | SB led to an average ↓ in K+ by 0.5 mEq/L at 30 minutes. Combination therapy with insulin/dextrose + salmeterol was more effective than SB. |
| Kim, 1996 | Observational n=12 | 8.4% SB 120 mEq/L x 1 hr Insulin drip 0.5 unit/kg/min x 1 hr | SB led to ↑ serum bicarbonate but no change in serum K+ (6.4 mEq/L to 6.3 mEq/L). Insulin drip led to ↓ serum K+ (6.3 mEq/L to 5.7 mEq/L). Combination of insulin drip + SB led to ↓ serum K+ (6.2 mEq/L to 5.2 mEq/L). |
| Blumberg, 1992 | Observational n=12 | 8.4% SB (240 mEq/hr) x 1 hr, then 1.4% 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 | Observational n=18 | 1.4% SB in H2O (1 mEq/kg) over 2 hrs 8.4% SB (1 mEq/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 | Observational n=10 | 8.4% SB drip x 1 hr 1.4% SB drip x 1 hr Epinephrine drip 0.05 mcg/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 | Observational n=14 | SB 89–134 mEq/1000 mL D5W over 4–6 hours D5W 1000 mL 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 series n=4 | 5% SB drip over 2–6 hours | Resolution of EKG abnormalities in all patients; 2/4 died within 24 hours. |
Conclusions
- Sodium bicarbonate, once considered a first-line agent for the transcellular shift of potassium, now has only a limited and controversial role in the acute treatment of hyperkalemia.
- Across the available studies, hypertonic sodium bicarbonate (the “amp of bicarb”) showed little to no acute potassium-lowering effect, while isotonic infusions produced only modest reductions, much of it attributable to extracellular volume expansion rather than a true intracellular shift.
- Insulin/dextrose, beta-2 agonists such as albuterol/salmeterol, and calcium remain the preferred agents for acute hyperkalemia; bicarbonate is best reserved as an adjunct, particularly in the setting of concurrent metabolic acidosis.
- When used, dosing, hypertonic versus isotonic formulation, and adverse effects (e.g., hypocalcemia, hypernatremia, hyperosmolality) should be weighed, and bicarbonate should not replace the more rapidly effective shift and stabilization therapies.
References
Sodium Bicarbonate. Micromedex [Electronic version]. Greenwood Village, CO: Truven Health Analytics. Retrieved August 29, 2019, 2018, from http://www.micromedexsolutions.com/
Gutierrez R et al. Miner Electrolyte Metab. 1991;17(5):297-302. [PMID: 1668124]
Fraley DS et al. Kidney Int. 1977 Nov;12(5):354-60. [PMID: 24132]
Blumberg A et al. Am J Med. 1988 Oct;85(4):507-12. [PMID: 3052050]
Blumberg A et al. Kidney Int. 1992 Feb;41(2):369-74. [PMID: 1552710]
Kim et al. Nephron. 1996;72(3):476-82. [PMID: 8852501]
Ngugi NN et al. East Afr Med J. 1997 Aug;74(8):503-9. [PMID: 9487416]
Long B et al. J Emerg Med. 2018 Aug;55(2):192-205. [PMID: 29731287]
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