Sodium Bicarbonate Use

OVERVIEW

  • metabolic acidosis leads to adverse cardiovascular effects
  • bicarbonate must be administered in a solution as sodium bicarbonate
  • 8.4% solution contains 1mmol of HCO3-/mL and is very hypertonic (2,000 mOsm/kg)
  • goal of NaHCO3 administration in severe metabolic acidosis to counteract the negative cardiovascular effects of acidaemia
  • alternatives to NaHCO3 include carbicarb, dichloroacetate, Tris/THAM

INDICATIONS

Accepted

  • Hyperkalaemia
  • Treatment of sodium channel blocker overdose (e.g. tricyclic overdose)
  • Urinary alkalinisation (salicylate poisoning)
  • Metabolic acidosis (NAGMA) due to HCO3 loss (RTA, fistula losses)

Controversial

  • Cardiac arrest (in prolonged resuscitation + documented severe metabolic acidosis)
  • Diabetic ketoacidosis (very rarely, perhaps if shocked and pH < 6.8)
  • Severe pulmonary hypertension with RVF to optimize RV function
  • Severe ischemic heart disease where lactic acidosis is thought to be an arrhythmogenic risk

ADVERSE EFFECTS

  • hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-)
  • hyperosmolality (cause arterial vasodilation and hypotension)
  • volume overload
  • rebound or ‘overshoot’ alkalosis
  • hypokalaemia
  • ionised hypocalcaemia
  • impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve
  • removal of acidotic inhibition of glycolysis by increased activity of PFK
  • CSF acidosis
  • hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis)
  • severe tissue necrosis if extravasation takes place
  • bicarbonate increases lactate production by:
    — increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis
    — shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues

POINTS TO REMEMBER WHEN USING BICARBONATE

  • it is generally better to correct underlying cause of acidosis and give supportive care than to give sodium bicarbonate
  • ensure adequate ventilation to eliminate CO2 produced
  • correct hypoxia — HCO3 may cause clinical deterioration if tissue hypoxia present due to removal of acidotic inhibition of glycolysis and leftward shift of the oxy-Hb dissociation curve
  • not useful in high anion gap acidosis (lactate and ketoacidosis – organic acids are metabolised thus regenerating HCO3 )
  • may be useful in correction of normal anion gap acidosis (non-organic acids do not have anions that can be metabolised to regenerate bicarbonate
  • the amount of HCO3 (mmol) to correct a NAGMA = 0.3 x weight x -SBE [-SBE = negative standard base excess)

CCC Pharmacology Series

LITFL

Journal articles

  • Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest. 2000 Jan;117(1):260-7. PMID: 10631227.
  • Omron EM, Omron RM. A physicochemical model of crystalloid infusion on acid-base status. J Intensive Care Med. 2010 Sep;25(5):271-80. PMID: 20622258.

FOAM and web resources

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at The Alfred ICU, where he is Deputy Director (Education). He is a Clinical Adjunct Associate Professor at Monash University, the Lead for the  Clinician Educator Incubator programme, and a CICM First Part Examiner.

He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives. He was one of the founders of the FOAM movement (Free Open-Access Medical education) has been recognised for his contributions to education with awards from ANZICS, ANZAHPE, and ACEM.

His one great achievement is being the father of three amazing children.

On Bluesky, he is @precordialthump.bsky.social and on the site that Elon has screwed up, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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