ResusDocDrug Monographs

Reference material for UK healthcare professionals. Doses and licensing change — verify against the current SmPC and local policy before use.

Drug monographs / Sodium bicarbonate

Sodium bicarbonate

A drug that was once given to almost every cardiac arrest, is now given to very few, and remains one of the most effective interventions in emergency medicine for the one poisoning it actually treats.

AntidoteToxicologyResuscitationElectrolytesCardiac arrest

At a glance

Strength8.4% = 1 mmol/mL sodium and bicarbonate
Adult dose (SmPC)1 mmol/kg, then 0.5 mmol/kg every 10 min
Children1 mmol/kg slow IV; dilute 1:1 in neonates
Key indicationTricyclic antidepressant overdose (licensed)
TCA triggerQRS widening, arrhythmia or hypotension
Not indicatedSepsis-related lactic acidosis; routine cardiac arrest
RequiresAdequate ventilation — CO₂ must be blown off
WatchAlkalosis, hypokalaemia, hypernatraemia, hypocalcaemia

Why this drug is interesting

Sodium bicarbonate has been through a complete reversal of clinical fortune. In the 1970s it was given routinely and early in cardiac arrest on the assumption that correcting the acidosis would restore responsiveness to catecholamines. It does not, and the practice was abandoned. What survived that retreat is a much smaller, much better-founded set of indications — and one of them, sodium channel blocker poisoning, is among the most reliably effective antidotal interventions in emergency medicine.

The interesting pharmacology is that in its best indication, bicarbonate is not primarily working as a buffer. It is working as a sodium load, with the alkalinisation as a second, complementary mechanism. Understanding that distinction is what stops clinicians from titrating it to a normal pH and stopping.

Pharmacology

Three separate mechanisms

Sodium loading
Raising extracellular sodium increases the electrochemical gradient across the myocyte membrane, driving sodium through the residual, unblocked fast sodium channels. This narrows the QRS and restores conduction in sodium-channel-blocker poisoning, and it is the dominant mechanism there.
Alkalinisation
Raising pH reduces drug binding to the sodium channel and increases the fraction of a weakly basic drug that is un-ionised and protein-bound rather than free. It also promotes the intracellular shift of potassium.
Buffering
Bicarbonate combines with hydrogen ions to form carbonic acid and then carbon dioxide and water. This is the mechanism people assume is primary, and it is the one that requires the patient to be able to ventilate.

Licensed indications and dosing

The UK licence for 8.4% sodium bicarbonate injection is narrower than its reputation suggests. It covers, in adults and children:1

  • Correction of metabolic acidosis associated with cardiac arrest in patients with pre-existing metabolic acidosis
  • Cardiac arrest associated with hyperkalaemia with pre-existing metabolic acidosis
  • Life-threatening hyperkalaemia with pre-existing metabolic acidosis
  • Tricyclic antidepressant overdose

The label adds that "sodium bicarbonate should only be used after other resuscitative measures such as cardiac compression, ventilation, adrenaline and antiarrhythmic agents have been attempted." Note how much work the phrase pre-existing metabolic acidosis is doing in the first three: bicarbonate is licensed for an acidosis that was already there, not for the one the arrest generated.

Dose

  • Adults: 1 mmol/kg (1 mL/kg of 8.4%), followed by 0.5 mmol/kg (0.5 mL/kg) at 10-minute intervals1
  • Children: 1 mmol/kg by slow intravenous injection
  • Premature infants and neonates: dilute the 8.4% solution 1:1 with 5% dextrose
  • Elderly: as for adults
  • Intravenous administration only. Check arterial or venous pH and CO₂ before and during treatment

Tricyclic antidepressant and sodium channel blocker poisoning

This is the indication that justifies the drug's continued place on the trolley. Tricyclic antidepressants block fast sodium channels in the myocardium, producing the characteristic progression: QRS widening, a rightward terminal QRS axis, then broad-complex arrhythmia, hypotension and arrest — layered on top of anticholinergic delirium and seizures.

The same logic elsewhere

Any sodium channel blocking poison produces the same ECG and responds to the same intervention: flecainide, quinine and chloroquine, cocaine-induced QRS prolongation, propranolol (which has membrane-stabilising activity that other beta-blockers lack), diphenhydramine and carbamazepine. In a poisoned patient with a broad QRS and no other explanation, bicarbonate is a reasonable move while the diagnosis is being worked out.

Where it does not belong

Routine cardiac arrest

Bicarbonate is not part of the standard adult ALS algorithm. Arrest acidosis is predominantly respiratory and hypoperfusion-driven; the treatment is effective chest compressions and ventilation. Its role in arrest is confined to the specific circumstances above — pre-existing metabolic acidosis, hyperkalaemia, and sodium channel blocker poisoning.

Diabetic ketoacidosis

Bicarbonate is not recommended in DKA at any pH in current UK practice. The acidosis resolves with fluid and insulin; bicarbonate has been associated with delayed ketone clearance, hypokalaemia and, in children, cerebral oedema. If someone is reaching for it in DKA, the question to ask is what problem they think it is solving.

Contraindications

  • Conditions where sodium intake is restricted — renal failure, hypertension, oedema, congestive cardiac failure
  • Hypoventilation — risk of worsening the acidosis
  • Metabolic or respiratory alkalosis
  • History of urinary calculi
  • Coexistent potassium or chloride depletion, hypocalcaemia, or hypernatraemia

Adverse effects and interactions

Adverse effects

  • Alkalosis, from overdose or over-enthusiastic repeat dosing
  • Hypokalaemia — potassium shifts intracellularly as pH rises; check it, and expect to replace it
  • Hypocalcaemia — alkalosis increases albumin binding and lowers ionised calcium, which can precipitate tetany or arrhythmia
  • Hypernatraemia and hyperosmolarity — 8.4% is a substantial sodium and osmolar load
  • Paradoxical intracellular acidosis where CO₂ cannot be cleared
  • Haemodynamic deterioration from volume overload
  • Intracranial haemorrhage in neonates; hyperirritability or tetany
  • Tissue necrosis on extravasation. The label warns specifically against using scalp veins

Interactions

Urinary alkalinisation increases the renal clearance of acidic drugs — salicylates (the basis of urinary alkalinisation in salicylate poisoning), doxycycline and other tetracyclines, chlorpropamide, lithium, methenamine. It increases the half-life and duration of action of basic drugs, including quinidine, amphetamines, ephedrine, pseudoephedrine, memantine and flecainide — a relationship worth noticing, since flecainide toxicity is also treated with bicarbonate.

Practical use in the ED

  1. Get an ECG in every significant overdose and measure the QRS. It is the trigger for this drug and the thing most often not looked at properly.
  2. Check ventilation before you give it. If the patient cannot increase minute ventilation, either they need to be intubated or the bicarbonate will make the intracellular pH worse.
  3. Give it as a bolus, and reassess the ECG. The response in sodium channel blockade is often visible within minutes; if the QRS is unchanged after adequate dosing, revisit the diagnosis.
  4. Check potassium and ionised calcium after dosing, not just the pH. Both fall, and both matter.
  5. Call NPIS. Infusion regimens, target pH and duration are decisions the label does not cover.

Critical appraisal

  1. The tricyclic indication rests on animal models, physiology and clinical experience, not randomised trials. It is one of the most confidently taught interventions in toxicology and one of the least trial-supported. The effect on the QRS is real and observable, which is unusual and reassuring; the effect on mortality is inferred.
  2. QRS thresholds are quoted with more precision than they deserve. The relationship between QRS duration and the risk of seizure or arrhythmia after tricyclic ingestion comes from a small number of observational studies, and the widely cited cut-offs are prognostic associations that have been converted into treatment thresholds by convention rather than by trial.
  3. Its fall from routine arrest use is a genuine success of evidence over mechanism, and worth teaching as such. The theory was excellent and the drug did not work. That pattern recurs — see metoprolol and COMMIT, or ketamine and intracranial pressure.
  4. The licensed indications are oddly narrow and rarely read. The requirement for pre-existing metabolic acidosis in the arrest indications is a meaningful restriction that almost nobody applies, and the sepsis statement in the label is more definite than most clinicians realise.

References

  1. 1
    Sodium Bicarbonate Injection BP 8.4% w/v — Summary of Product Characteristics, Martindale Pharma. electronic Medicines Compendium. Sections 4.1–4.5, 4.8. Source of the indications, doses, contraindications and the sepsis statement. Verified 23 Aug 2026.
  2. 2
    Sodium Bicarbonate 8.4% w/v solution for infusion — Summary of Product Characteristics, B.Braun Medical. electronic Medicines Compendium
  3. 3
    TOXBASE — tricyclic antidepressants; sodium bicarbonate. National Poisons Information Service. toxbase.org (NHS login required. NPIS: 0344 892 0111. The authoritative UK source for infusion regimens and target pH, which the product licence does not cover.)
  4. 4
    Bruccoleri RE, Burns MM. A literature review of the use of sodium bicarbonate for the treatment of QRS widening. J Med Toxicol 2016;12(1):121–9. PubMed
  5. 5
    Resuscitation Council UK. 2025 Adult Advanced Life Support and Newborn Life Support Guidelines. resus.org.uk — local copies at lifesupport.resusdoc.uk
  6. 6
    Sodium bicarbonate — dosing and safety monograph. BNF, NICE. bnf.nice.org.uk

Last reviewed 2026-08-24 · Author: Dr Nirmalya Hore