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Sodium Bicarbonate

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Last Update: March 11, 2023.

Continuing Education Activity

Sodium bicarbonate is a medication used in the management and treatment of multiple disease pathologies. It is a general chemical compound by classification. This activity outlines and reviews the indications, action, and contraindications for sodium bicarbonate as a valuable agent in the treatment, management, and therapy of lactic acidosis, QRS prolongation, and other disorders when applicable. This activity will highlight the mechanism of action, adverse event profile, and other key factors, e.g., dosing, toxicities, contraindications, and relevant interactions pertinent for healthcare team members in managing several conditions.


  • Identify the mechanism of action of sodium bicarbonate.
  • Describe the potential adverse effects of sodium bicarbonate.
  • Review appropriate monitoring for patients receiving sodium bicarbonate.
  • Outline interprofessional team strategies for improving sodium bicarbonate toxicity monitoring.
Access free multiple choice questions on this topic.


Sodium bicarbonate is a chemical compound made of sodium (Na+) and bicarbonate (HCO3-), for which the indications are many.

FDA approved indications include:

  • Cardiac conduction delays
  • QRS prolongation (ex. tricyclic antidepressant poisoning)

Under arrhythmias and cardiovascular instability, sodium bicarbonate can be administered to adults at 4 to 8 hour IV infusions. Each dose should be monitored and planned in a standard protocol to help evaluate the degree of response expected and predicted to understand the necessity to advance further infusions or withhold administration, given its fluid overloading effects. 

Metabolic acidosis, related to:

  • Severe renal disease
  • Uncontrolled diabetes
  • Severe primary lactic acidosis[1][2][3]
  • Circulatory insufficiency due to shock
  • Severe dehydration
  • Extracorporeal circulation of blood
  • Cardiac arrest
  • Drug toxicities
  • Barbiturates
  • Salicylate
  • Toxic alcohols[4]
  • Urine alkalization[5]
  • Severe diarrhea with HCO3 loss

Non-FDA approved indications: 

Nebulized sodium bicarbonate is an excellent option to treat chemical injuries resulting from chlorine gas, especially within the pulmonary mucosa. The belief is that the inhaled gas neutralizes when it reacts with water and bicarbonate within the respiratory system.[6] 

Mechanism of Action

After administration, intravenous sodium bicarbonate dissociates to form sodium (Na) and bicarbonate (HCO3). Bicarbonate anions can consume hydrogen ions (H) and subsequently convert to carbonic acid (H2CO3). Carbonic acid subsequently converts to water (H2O) and carbon dioxide (CO2) for excretion from the lungs. The main therapeutic effect of sodium bicarbonate administration is increasing plasma bicarbonate levels, which are known to buffer excess hydrogen ion concentration, thereby raising solution pH to combat clinical manifestations of acidosis.

Bicarbonate is often a standard element of body fluids and is often regulated by the kidney via secretion or absorption methods to counter-regulate changes in serum pH. This action often leads to its second administration as it is known to alkalinize the urine, capable of changing precipitants in urine and providing a means of normalizing tubular acid concentration gradients to manage high fluctuations in serum acid-base status changes. This alkalization process enables compounds that would normally precipitate in the renal tubules in acidic conditions to be buffered within the renal tubule, thereby preventing mechanical or chemical damage while also providing increased efficiency within the kidney tubules to excrete acidified substances without disrupting the electrochemical gradient.[7][4]


NaHCO3 comes in various forms, including oral tablets, IV injections, and IV infusions.

Oral formulations are available via powder, 325 mg, and 650 mg oral tablets.

1 mEq NaHCO3 is 84 mg. 1000 mg = 1 gram of NaHCO3 contains 11.9 mEq of sodium and bicarbonate ions. One 650 mg tablet of NaHCO3 has 7.7 mEq of sodium and bicarbonate ions.

The two primary IV injection formulations of NaHCO3 are as follows:

  • 7.5% concentration = 44.6 mEq NaHCO3 in 50 mL. 7.5% concentration supplies 75 mg/mL, which also consists 0.9 mEq/mL for each sodium and bicarbonate.
  • 8.4% concentration = 50 mEq in 50 mL. 8.4% concentration supplies 84 mg/mL, which also consists 1 mEq/mL for each sodium and bicarbonate. One ampoule of 50 ml contains 50 mEq sodium and 50 mEq bicarbonate to a total of 100 mEq/50 mL and corresponds to 2000 mosm per liter. This formulation is a hypertonic solution and can raise serum sodium concentration with the attraction of water to the extracellular areas from the intracellular area.
  • A 4.2% and 5% solution are also available, though not as often used given the dosing availability of larger concentrations. 

NaHCO3 IV infusions are available in the following formulations:

  • 50 mEq, 75 mEq, 100 mEq NaHCO3 in 1L of 0.45% NS, 0.45%NS+D5W, or D5W
  • 50 mEq, 75 mEq, 100 mEq and 150 mEq NaHCO3 in 1L D5W or Sterile water
  • Bicarbonate tablets are available as 650mg NaHCO3, 25 to 50 mEq KHCO3, 20 to 40 mEq KHCO3-citric acid, and 20 to 50 mEq KHCO3-KCl tablets.[8]

Common Uses of Sodium Bicarbonate

Cardiac arrest: Currently, routine bicarbonate administration for cardiac arrest is no longer a recommendation. It should only be administered for cardiac arrest due to hyperkalemia or tricyclic antidepressant overdose, or metabolic acidosis.[9] Dosing is 1 mEq/kg per dose, repeated according to arterial blood gas measurements. Sodium bicarbonate should ideally be given after adequate alveolar ventilation and the initiation of cardiac compressions.

Acute metabolic acidosis: If pH is less than 7.1 or pH less than 7.1 to 7.2 in patients with severe acute kidney injury (oliguria or 2-fold or larger increase in serum creatinine level)

Chronic metabolic acidosis: 50 to 100 mEq oral tablet can be initiated and titrated according to the ongoing evaluation of acid-base balance.

Lactic acidosis: The use of sodium bicarbonate remains controversial but is an option if pH is below 7.[10]

Diabetic ketoacidosis: The use of sodium bicarbonate remains controversial in diabetic ketoacidosis since recovery outcome is similar with or without NaHCO3. However, sodium bicarbonate is still recommended if the pH is below 7 after 1 hour of fluid administration. Sodium bicarbonate should be given in hypotonic fluid every two hours until pH is at least 7.[11]

Hyperkalemia: When patients with severe hyperkalemia (serum potassium level of more than 6 mEq/L or more than 5.5 mEq/L with arrhythmia or EKG changes) have metabolic acidosis, sodium bicarbonate should be administered. The dose needed is empirical and is unpredictable. Initially, 150 mEq of sodium bicarbonate can be given in 1 liter of 5% dextrose over 4 hours. More can be given if acidosis does not correct with this regimen.[12] If there is a need to decrease serum potassium emergently, 50 mEq of NaHCO3 IV can be given over 5 minutes, followed by other methods of potassium reduction.

Sodium bicarbonate administration can be at varying doses for renal tubular acidosis, and to achieve urine alkalization, it can be given IV for some intoxications such as salicylate overdose and as a preventative measure against contrast-induced nephropathy.

Adverse Effects

Sodium bicarbonate can result in a multitude of adverse effects, including:

  • Metabolic alkalosis
  • Headache
  • Muscle pain and twitching
  • Nausea or vomiting
  • Bradypnea
  • Nervousness or restlessness
  • Unpleasant taste
  • Increased frequency in urination
  • Tissue damage/necrosis secondary to extravasation[13][10]

Administration and extravasation of sodium bicarbonate have been known to cause chemical cellulitis due to its basic properties and have resulted in tissue necrosis, ischemia, and tissue death at administration sites. 

In large dose administrations, it is known to increase edema and is more commonly noted in those with renal insufficiency, given its clearance via the kidneys. This increase in tissue edema appears to be due to an excess hyperosmolar state developed during the administration of sodium bicarbonate resulting in fluid retention. This condition can be especially challenging to manage in those with underlying cardiovascular comorbidities, including those with heart failure with intravascular fluid management difficulties. 


Due to rapid alkalotic effects, sodium bicarbonate is contraindicated in those with signs/symptoms or laboratory values indicating underlying metabolic or respiratory alkalosis due to the potential for exacerbation of symptoms.

Secondary to deionizing effects on metabolically active ionized serum calcium, sodium bicarbonate is contraindicated in patients with hypocalcemia.

Due to its ability to buffer pH and influence acid-base shifts, sodium bicarbonate can also influence a multitude of drug-drug interactions. These include:

  • Antibiotics
    • Doxycycline, levofloxacin, minocycline, tetracyclines

These effects are often noted in oral preparations where both medications are taken orally and result in significantly decreased GI absorption due to compound structural alterations due to changes in pH in the GI lumen.

  • NSAIDs/other related anti-inflammatory medications
  • Mesalamine, sulfasalazine

These interactions are due to the effects of sodium bicarbonate on increasing renal tubular pH, thereby increasing passive tubular reabsorption and increasing serum levels of medication.

The administration of sodium bicarbonate can exacerbate hypernatremia.

Rapid or high-dose administration of undiluted sodium bicarbonate may lead to decreased CSF pressure and intracranial hemorrhage, particularly in the pediatric population under the age of 2.

Another contraindication is for those that have hypersensitivity to sodium bicarbonate injections.[4][14]


Clinicians should monitor serum electrolytes, including calcium, urinary pH, and when indicated, arterial blood gases.


Rapid administration of sodium bicarbonate may increase intravascular fluid volume, leading to acute pulmonary edema. Additionally, the medication must be administered judiciously in those with congestive heart failure, significant renal disease, or sodium retention due to exacerbation of sodium retention and edema.

Sodium bicarbonate administration in a rapid infusion or as large boluses can result in acute metabolic alkalosis resulting in reduced serum ionized calcium. This acute shift in ionized calcium can result in tetany. This severe alkalosis is potentially treatable with ammonium chloride. Hypocalcemia may be addressed with calcium gluconate. An addition of 0.9 % NS infusion and potassium supplementation may also be indicated.[15][16]

Enhancing Healthcare Team Outcomes

Appropriate use of sodium bicarbonate and preventing its potential adverse effects require the involvement of the entire allied interprofessional team of healthcare professionals. When ordering sodium bicarbonate for a patient, the ordering/prescribing clinician, administering nursing team, and pharmacy team must recognize the indications for the medication and observe any toxicity or side effects from its administration. Clinicians need to ensure that sodium bicarbonate is the appropriate therapeutic choice. Nursing will either administer the drug if the patient is inpatient or give instructions for home administration for outpatient use and counsel regarding potential adverse events. Pharmacists will verify appropriate dosing, perform medication reconciliation checking for drug-drug interactions, and reinforce patient counseling points where appropriate. Utilizing an interprofessional approach to sodium bicarbonate therapy will increase the chances of therapeutic success while minimizing adverse events, which will result in better patient outcomes. [Level 5]

Despite consistent, systematic checkpoints in evaluating negative outcomes, the clinical observation and recognition at the bedside consistently improve morbidity and mortality in the setting of patient medication errors, medication-induced reactions, and side effects. 

Review Questions


Adeva-Andany MM, Fernández-Fernández C, Mouriño-Bayolo D, Castro-Quintela E, Domínguez-Montero A. Sodium bicarbonate therapy in patients with metabolic acidosis. ScientificWorldJournal. 2014;2014:627673. [PMC free article: PMC4227445] [PubMed: 25405229]
Lutterman JA, Adriaansen AA, van 't Laar A. Treatment of severe diabetic ketoacidosis. A comparative study of two methods. Diabetologia. 1979 Jul;17(1):17-21. [PubMed: 38163]
Arieff AI. Indications for use of bicarbonate in patients with metabolic acidosis. Br J Anaesth. 1991 Aug;67(2):165-77. [PubMed: 1653584]
Mirrakhimov AE, Ayach T, Barbaryan A, Talari G, Chadha R, Gray A. The Role of Sodium Bicarbonate in the Management of Some Toxic Ingestions. Int J Nephrol. 2017;2017:7831358. [PMC free article: PMC5591930] [PubMed: 28932601]
Erejuwa OO, Aja DOJ, Uwaezuoke NI, Nwadike KI, Ezeokpo BC, Akpan JL, Nwobodo NN, Araromi E, Asika E. Effects of honey supplementation on renal dysfunction and metabolic acidosis in rats with high-fat diet-induced chronic kidney disease. J Basic Clin Physiol Pharmacol. 2020 May 12; [PubMed: 32396139]
Cevik Y, Onay M, Akmaz I, Sezigen S. Mass casualties from acute inhalation of chlorine gas. South Med J. 2009 Dec;102(12):1209-13. [PubMed: 20016425]
Pentel P, Benowitz N. Efficacy and mechanism of action of sodium bicarbonate in the treatment of desipramine toxicity in rats. J Pharmacol Exp Ther. 1984 Jul;230(1):12-9. [PubMed: 6086872]
Spivey WH, Lathers CM, Malone DR, Unger HD, Bhat S, McNamara RN, Schoffstall J, Tumer N. Comparison of intraosseous, central, and peripheral routes of sodium bicarbonate administration during CPR in pigs. Ann Emerg Med. 1985 Dec;14(12):1135-40. [PubMed: 2998236]
Velissaris D, Karamouzos V, Pierrakos C, Koniari I, Apostolopoulou C, Karanikolas M. Use of Sodium Bicarbonate in Cardiac Arrest: Current Guidelines and Literature Review. J Clin Med Res. 2016 Apr;8(4):277-83. [PMC free article: PMC4780490] [PubMed: 26985247]
Boyd JH, Walley KR. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? Curr Opin Crit Care. 2008 Aug;14(4):379-83. [PubMed: 18614899]
Chiasson JL, Aris-Jilwan N, Bélanger R, Bertrand S, Beauregard H, Ekoé JM, Fournier H, Havrankova J. Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ. 2003 Apr 01;168(7):859-66. [PMC free article: PMC151994] [PubMed: 12668546]
Abuelo JG. Treatment of Severe Hyperkalemia: Confronting 4 Fallacies. Kidney Int Rep. 2018 Jan;3(1):47-55. [PMC free article: PMC5762976] [PubMed: 29340313]
El-Solh AA, Abou Jaoude P, Porhomayon J. Bicarbonate therapy in the treatment of septic shock: a second look. Intern Emerg Med. 2010 Aug;5(4):341-7. [PubMed: 20169423]
Łoniewski I, Wesson DE. Bicarbonate therapy for prevention of chronic kidney disease progression. Kidney Int. 2014 Mar;85(3):529-35. [PubMed: 24107852]
Geng X, Yu J, Xu J, Jin S, Shao W, Wang Y, Guo M, Cao X, Zou J, Xu X, Ding X. Role of magnesium in the risk of intradialytic hypotension among maintenance hemodialysis patients. Hemodial Int. 2020 Jul;24(3):351-358. [PubMed: 32395903]
Koski C, Sarkar N, Bose S. Cytotoxic and osteogenic effects of crocin and bicarbonate from calcium phosphates for potential chemopreventative and anti-inflammatory applications in vitro and in vivo. J Mater Chem B. 2020 Mar 11;8(10):2048-2062. [PubMed: 32064472]

Disclosure: Niluk Leon Senewiratne declares no relevant financial relationships with ineligible companies.

Disclosure: Allison Woodall declares no relevant financial relationships with ineligible companies.

Disclosure: Ahmet Can declares no relevant financial relationships with ineligible companies.

Copyright © 2023, StatPearls Publishing LLC.

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Bookshelf ID: NBK559139PMID: 32644565


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