Sodium Bicarbonate | Medication Reference

Bedside Snapshot

Core Use: Acute treatment of (1) severe metabolic acidosis, (2) hyperkalemia with acidosis, and (3) toxicologic emergencies involving sodium-channel blockers (e.g., TCA overdose) and salicylate toxicity
Standard Adult Amp: 8.4% sodium bicarbonate = 50 mEq (mmol) of NaHCO₃ in 50 mL (1 mEq/mL); hypertonic with substantial sodium load
Onset: Immediate pH effect in blood, but depends on adequate ventilation (bicarbonate → CO₂ which must be exhaled)
Key Danger: Without adequate ventilation, can worsen intracellular/CNS acidosis; also risk hypernatremia, volume overload, metabolic alkalosis, hypokalemia, and hypocalcemia
Special Note: NOT routinely recommended for cardiac arrest or lactic acidosis unless specific indication (e.g., hyperkalemia, TCA overdose) present

Brand & Generic Names

Generic Name: Sodium bicarbonate
Brand Names: Generic formulations; sometimes labeled as 8.4% sodium bicarbonate injection

Medication Class

Systemic alkalinizing agent; buffer; hypertonic sodium salt; antidotal therapy in select toxicologic emergencies

Pharmacology

Mechanism of Action:

Sodium bicarbonate dissociates into Na⁺ and HCO₃⁻ in plasma
Bicarbonate buffers excess hydrogen ions: H⁺ + HCO₃⁻ ↔ H₂CO₃ ↔ CO₂ + H₂O, raising blood pH when CO₂ is removed via ventilation
In hyperkalemia, alkalinization shifts potassium into cells (H⁺ moves out, K⁺ moves in to preserve electroneutrality)
In TCA/sodium-channel–blocking overdoses: (1) serum alkalinization decreases drug binding to sodium channels, and (2) sodium load helps overcome sodium-channel blockade in cardiac tissue
In salicylate toxicity, serum alkalinization reduces CNS penetration (ion trapping), and urine alkalinization enhances renal excretion
Excessive use can lead to metabolic alkalosis, decreased ionized calcium, decreased cerebral blood flow, and left shift of oxyhemoglobin dissociation curve

Pharmacokinetics:

Onset: Rapid (minutes) after IV bolus for serum pH change; full equilibration depends on ventilation
Distribution: Bicarbonate largely remains in extracellular fluid initially; sodium stays extracellular unless transported across cell membranes
Metabolism: Bicarbonate participates in normal CO₂/HCO₃⁻ physiology; excess bicarbonate generates CO₂ that must be eliminated via lungs
Elimination: Excess bicarbonate and sodium excreted via kidneys; effect prolonged in renal failure, increasing risk of volume overload and electrolyte disturbances

Indications

Severe metabolic acidosis with hemodynamic compromise (e.g., pH ≤7.1) when underlying cause is being treated and acidosis is thought to be harmful or not rapidly reversible
Hyperkalemia with ECG changes or severe hyperkalemia (as adjunct to calcium, insulin/dextrose, and beta-agonists), especially when significant metabolic acidosis is present
Toxicologic emergencies: tricyclic antidepressant overdose and other sodium-channel–blocking agents with QRS widening, ventricular dysrhythmias, or hypotension
Salicylate (aspirin) toxicity requiring serum/urine alkalinization while preparing for or performing hemodialysis
Selected cases of rhabdomyolysis or crush injury where urine alkalinization is used as part of a kidney-protection strategy
Renal tubular acidosis and chronic metabolic acidosis (usually managed with oral bicarbonate or alkali therapy, not acute IV bicarb)

Dosing & Administration

Available Forms:

8.4% sodium bicarbonate injection (adult/standard): 1 mEq/mL; each 50 mL vial/"amp" contains 50 mEq of NaHCO₃ in sterile water
4.2% sodium bicarbonate (pediatric or diluted form): 0.5 mEq/mL, often used in neonates/infants or when a less hypertonic solution is desired
Isotonic bicarbonate infusion: e.g., 150 mEq NaHCO₃ in 1 L D5W, approximating isotonicity for continuous infusion
Custom mixtures for salicylate toxicity: commonly 150 mEq NaHCO₃ plus 40 mEq KCl in 1 L D5W per local toxicology protocol

Dosing – Sodium Bicarbonate (Adult IV, always follow local protocol):

Indication / Scenario	Typical Dose	Administration	Notes
Severe metabolic acidosis (pH ≤7.1)	1–2 mEq/kg IV (e.g., 50–100 mEq)	Slow IV push over 5–10 min or short infusion	Give partial calculated dose and reassess ABG/VBG; avoid overcorrection
Ongoing metabolic acidosis – infusion	150 mEq NaHCO₃ in 1 L D5W	Infuse 100–250 mL/h, titrated to pH	Consider formula: dose (mEq) ≈ 0.5 × weight (kg) × base deficit; give 1/2 to 1/3 initially
Hyperkalemia (with acidosis)	50 mEq (1 amp) IV	Over 5–10 min; may repeat in 5–10 min if needed	Effect on K⁺ modest and transient; prioritize calcium, insulin/dextrose, beta-agonists
TCA overdose – initial bolus	1–2 mEq/kg IV (50–100 mEq)	Rapid IV push over 1–2 min in unstable patients	Repeat until QRS <120 ms and/or pH ~7.50–7.55
TCA overdose – infusion	150 mEq NaHCO₃ in 1 L D5W	Run at 150–250 mL/h and titrate	Maintain pH ~7.50–7.55 and narrow QRS; involve toxicology
Salicylate toxicity	1–2 mEq/kg IV bolus, then 150 mEq NaHCO₃ + 40 mEq KCl in 1 L D5W at 150–250 mL/h	Bolus then continuous infusion	Target serum pH 7.45–7.55 and urine pH ≥7.5
Rhabdomyolysis / crush	150 mEq NaHCO₃ in 1 L D5W	100–200 mL/h with high-volume resuscitation	Evidence mixed; ensure adequate volume, monitor closely

Contraindications

Contraindications (relative in the context of life-threatening emergencies):

Metabolic or respiratory alkalosis
Hypernatremia or severe volume overload (e.g., decompensated heart failure) where additional sodium load is hazardous
Hypocalcemia (ionized) that is symptomatic or clinically significant, as alkalosis further lowers ionized calcium and may precipitate tetany or arrhythmias

Major Precautions:

Inadequate ventilation: Bicarbonate administration increases CO₂; if ventilation is not increased, intracellular and CNS acidosis can worsen even as blood pH rises
Lactic acidosis and cardiac arrest: Routine use of bicarbonate is NOT recommended; consider only when specific indications (e.g., hyperkalemia, TCA overdose, known pre-existing metabolic acidosis) are present
Renal failure: Impaired excretion of sodium and bicarbonate increases risk of volume overload, hypernatremia, and metabolic alkalosis; use lower doses and close monitoring
Hypokalemia and hypocalcemia: Alkalosis shifts K⁺ into cells and decreases ionized calcium, potentially triggering arrhythmias or tetany, especially when combined with other therapies
Extravasation: Hypertonic solutions can cause local tissue irritation or damage; ensure reliable IV access and consider central access for large or repeated doses/infusions

Adverse Effects

Common:

Volume expansion and mild hypernatremia after repeated dosing
Metabolic alkalosis if overcorrected
Hypokalemia (K⁺ shift into cells)
Decreased ionized calcium and possible neuromuscular irritability
Local irritation or pain at injection site

Serious:

Severe hypernatremia and volume overload leading to pulmonary edema or heart failure
Significant metabolic alkalosis with decreased cerebral blood flow and impaired oxygen unloading
Paradoxical intracellular and CNS acidosis if CO₂ is not effectively cleared
Arrhythmias or tetany from abrupt changes in electrolytes (K⁺, Ca²⁺)
Tissue necrosis with large extravasations of hypertonic bicarbonate

Special Populations

Renal Impairment:

Reduced ability to excrete sodium and bicarbonate increases risk of fluid overload, hypernatremia, and alkalosis
Use with extreme caution; consider reduced doses and frequent monitoring of electrolytes, volume status, and acid-base balance

Hepatic Impairment:

No direct hepatic metabolism of bicarbonate, but patients with severe liver disease may have complex acid-base disorders
Monitor closely and address underlying metabolic derangements

Pregnancy & Lactation:

Sodium bicarbonate may be used in pregnancy when clinically indicated for life-threatening conditions (e.g., severe acidosis, toxicologic emergencies)
Consider maternal-fetal acid-base physiology and consult obstetrics when appropriate

Elderly:

Increased risk of volume overload, heart failure, and electrolyte disturbances
Use conservative dosing and monitor closely

Monitoring

Laboratory Monitoring:

Serial ABG/VBG for pH, PaCO₂, and bicarbonate levels; reassess after each bolus or dose change
Serum electrolytes: Na⁺, K⁺, Cl⁻, Ca²⁺ (ionized), Mg²⁺, and lactate as appropriate
Renal function and urine output, especially with repeated doses or continuous infusions
Urine pH in salicylate toxicity and urine alkalinization protocols

Clinical Monitoring:

Continuous ECG for QRS duration, QT interval, and arrhythmias in toxicology and hyperkalemia cases
Volume status and signs of pulmonary edema or heart failure (JVP, lung exam, oxygenation)
Ventilator parameters and capnography to ensure adequate CO₂ clearance
Neurologic status and signs of tetany or neuromuscular irritability

Clinical Pearls

Standard Amp: Remember that one standard adult amp of 8.4% sodium bicarbonate = 50 mEq in 50 mL. For quick mental math: 1 mEq/mL.

TCA Overdose: In TCA overdose with wide QRS, don't delay bicarbonate while waiting for levels—early, aggressive boluses are life-saving; watch QRS and pH as your endpoints.

Hyperkalemia: Bicarbonate is an adjunct, not a primary therapy for hyperkalemia. Calcium, insulin/dextrose, beta-agonists, and dialysis are your core tools for stabilizing and removing potassium.

Avoid Chasing Labs: Avoid chasing 'normal' bicarbonate levels—treat the patient and their hemodynamics, not just the lab value. Overcorrection to alkalosis can do harm.

Think CO₂: Whenever you push bicarb, think about CO₂. Ensure your patient can blow it off (spontaneously or via the ventilator), or you risk worsening intracellular and CNS acidosis.

References

1. Kraut, J. A., & Kurtz, I. (2001). Use of base in the treatment of severe acidemic states. American Journal of Kidney Diseases, 38(4), 703–727.
2. Kraut, J. A., & Madias, N. E. (2014). Lactic acidosis. New England Journal of Medicine, 371(24), 2309–2319.
3. American Heart Association. (2020). 2020 AHA Guidelines for CPR and Emergency Cardiovascular Care.
4. Haley, M., & Albertson, T. (2019). Tricyclic antidepressant poisoning: Clinical manifestations, diagnosis, and management. Emergency Medicine Clinics of North America, 37(2), 185–204.
5. EMCrit Project. (2023). Metabolic acidosis (IBCC). https://emcrit.org/ibcc/metabolic-acidosis/