- 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
- Treatment of sodium channel blocker overdose (e.g. tricyclic overdose)
- Urinary alkalinisation (salicylate poisoning)
- Metabolic acidosis (NAGMA) due to HCO3 loss (RTA, fistula losses)
- 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
- hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-)
- hyperosmolality (cause arterial vasodilation and hypotension)
- volume overload
- rebound or ‘overshoot’ alkalosis
- 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)
References and links
- 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
- EMCrit Podcast 50 – Acid Base Part IV – Choose the Solution Based on the Problem
- EMCrit Podcast 97 – Acid-Base VI – Chloride-Free Sodium
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health, a Clinical Adjunct Associate Professor at Monash University, and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of LITFL.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of two amazing children.
On Twitter, he is @precordialthump.