- A metabolic acidosis is a process which, if uncorrected, would lead to an acidaemia.
- It is usually associated with a low bicarbonate concentration (or total CO2), but an acidosis may be masked by a co-existing metabolic alkalosis.
- accumulation of acids (measured, i.e. chloride hyperchloraemic metabolic acidosis] or unmeasured [increased anion gap metabolic acidosis])
- renal or gastrointestinal loss of bicarbonate (with absorption of chloride, resulting in hyperchloraemic metabolic acidosis).
ANION GAP AND METABOLIC ACIDOSIS
Anion gap = (Na + K) – (Cl + HCO3) simplified as (Na) – (Cl + HCO3)
- is usually determined primarily by negatively charged plasma proteins
- range = 10 to 16 mmol/L (8 to 12 mmol/L if K not included)
- AG decreases by about 2.5 mmol/L for every decrease in albumin by 10 g/L
- increased anion gap -> fall in unmeasured cations (Ca, Mg) or increase in unmeasured anions (lactate, ketoacids, formate (methanol), glycolate and oxlate (ethylene glycol))
High anion gap (HAGMA)
- Toxins – methanol, metformin, phenformin, paraldehyde, propylene glycol, pryroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salcylates, solvents
Normal anion gap (NAGMA)
- Acetazolamide and Addisons
- GI causes – diarrhoea, vomiting, fistulas (pancreatic, ureterostomies, small bowel, ileostomies)
- Extras – RTA
- Check delta ratio in HAGMA to determine if there is a coexistant NAGMA.
- osmolar gap can help as a screening test for methanol or ethylene glycol intoxication once alcohol has been excluded (calculated osmolality = 2*Na + Glucose + Urea + ethanol/4.6).
- urinary pH (inappropriately alkaline for an acidaemia) and electrolytes may facilitate eliciting the specific cause of the renal bicarbonate loss (e.g. renal tubular acidosis).
References and Links
- Acid-Base: ABG analysis – Anion Gap – SID – NAGMA
- Metabolic acidosis: Overview – evaluation – DDx
- Metabolic alkalosis: Overview – evaluation – DDx
- Respiratory acidosis: Overview – DDx
- Respiratory alkalosis: Overview – DDx
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.