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 when the inhaled gas neutralizes when it reacts with water and bicarbonate within the respiratory system.[6] 

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 in 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 urine that's capable of changing precipitants in urine as well as 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 made 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 due to tricyclic antidepressant overdose or in 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: 50-100 mEq oral tablet can be initiated and titrated according to the ongoing evaluation of acid-base balance.

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

Diabetic ketoacidosis: Use of sodium bicarbonate remains controversial in diabetic ketoacidosis since recovery outcome is similar with or without NaHCO3. However, sodium bicarbonate is still a recommendation 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 like salicylate overdose and to prevent contrast-induced nephropathy.

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 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 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 those 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]