Sodium Bicarbonate

• 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

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

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

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

• 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)

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):

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

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

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

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

• 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/