Sodium Bicarbonate
Brand names: Minijet Sodium Bicarbonate, Sodium Bicarbonate 8.4%
Sodium bicarbonate is an alkalinising agent used intravenously to treat severe metabolic acidosis and, in specific settings, to manage hyperkalaemia and certain drug toxicities.
Adult dose
Paediatric dose
Dose independently re-sourced from UK Summary of Product Characteristics (SPC) via the eMC; US FDA prescribing information (openFDA / DailyMed) — cross-check; US labelling may differ from UK — clinician-reviewed. Always confirm against the product SmPC and your local formulary before prescribing.
UNIT IS mmol, NOT mg — do not convert or assume milligrams. SPC section 4.2 Paediatric population: 'The dosage has to be adjusted individually. The first dose can be up to 1 mmol/kg body weight, administered by slow intravenous infusion. In newborns and children under 2 years: the daily dose should not exceed 5 mmol per kg body weight per day, administered by slow intravenous infusion.' The 1 mmol/kg figure is an UPPER LIMIT for the first dose ('can be up to'), not a fixed dose. 1 mmol corresponds to 1 ml of the 8.4% w/v solution. In newborns and children under 2 years, 4.2% w/v (or less concentrated) sodium bicarbonate solutions should be preferred, and rapid infusion (10 ml/min) of hypertonic sodium bicarbonate solutions may produce hypernatraemia, a decrease in cerebrospinal fluid pressure and (in preterm infants) possible intracranial haemorrhage. For urine alkalinisation the SPC gives a bolus of 1-2 mmol/kg for haemodynamically stable adults AND children — see adultDose.notes. Verify against a children's formulary before prescribing.
Contraindications
- Hypersensitivity to the active substance or to any of the excipients
- Respiratory and metabolic alkalosis
- Hypoventilation (risk of worsening acidosis)
- Hypernatraemia
- Hypokalaemia
- Excessive chloride loss
Side effects
- Hypernatraemia (frequency not known)
- Serum hyperosmolarity (frequency not known)
- Tissue necrosis following paravenous administration
- Vein irritation with consequent phlebitis or thrombosis if infused undiluted or too rapidly into peripheral veins (stated in SPC section 4.4)
- Hypokalaemia — alkalinisation or correction of acidosis promotes potassium influx into cells (stated in SPC section 4.4)
Interactions
- Urine alkalinisation by sodium bicarbonate accelerates the elimination of acidic drug substances, e.g. acetylsalicylic acid, and delays the elimination of basic drug substances
- May interact with gluco- and mineralocorticoids, androgens and diuretics, increasing potassium excretion
Clinical monograph
How it works
Bicarbonate ions buffer excess hydrogen ions, raising blood pH, while also promoting an intracellular shift of potassium.
Prescribing in practice
- Rapid or excessive administration can cause metabolic alkalosis, hypokalaemia, hypernatraemia, fluid overload and a fall in ionised calcium, so it should be reserved for clearly indicated severe acidosis.
- It is hypertonic and irritant, and extravasation can cause tissue damage; large-vein or central administration is preferred for concentrated solutions.
- It is incompatible with calcium-containing solutions and many other drugs, which may precipitate in the line.
Monitoring
Monitor arterial blood gases, serum electrolytes including potassium and sodium, and acid-base status during therapy.
Counselling the patient
- Inform the team that the infusion site should be checked for extravasation.
- Advise that potassium and pH are rechecked to guide further dosing.
Evidence & guidelines
Its role is supported by acute care and resuscitation guidance, which generally restricts use to severe acidosis and specific indications rather than routine correction.
Reference: Resuscitation Council UK ALS 2021; TOXBASE; Drug verified in RxNorm (NLM); confirm dosing against the manufacturer SPC (eMC). Verify against your local formulary and current prescribing references before prescribing. The structured dose values shown have been reviewed by a clinician. Monograph status: clinician-reviewed (2026-07-04).
Related
Curated clinical cross-links plus same-class fallbacks.