- a metabolic acidosis is an abnormal primary process or condition leading to an increase in fixed acids in the blood -> resulting in a fall in arterial plasma bicarbonate
- pathophysiological mechanism:
- (i) A gain of strong acid
- (ii) A loss of base
- the gain of strong acid may be endogenous (eg ketoacids from lipid metabolism) or exogenous (NH4Cl infusion).
- bicarbonate loss may occur via the bowel (diarrhoea, small bowel fistulas) or via the kidneys (carbonic anhydrase inhibitors, renal tubular acidosis).
High anion gap (HAGMA)
- Toxins – methanol, metformin, phenformin, paraldehyde, propylene glycol, pyroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salicylates, solvents
Normal anion gap (NAGMA)
- Acetazolamide and Addisons
- GI causes – diarrhoea, vomiting, fistulas (pancreatic, ureterostomies, small bowel, ileostomies)
- Extras – RTA
- the disorder is maintained as long as the primary cause persists.
- in many cases the acid-base disturbance tends to increase in severity while the problem causing it persists though this is not absolute.
- hyperventilation (Kussmaul respirations) – this is the compensatory response
- shift of oxyhaemoglobin dissociation curve (ODC) to the right – due to the acidosis occurs rapidly
- decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) -> after 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal.
- depression of myocardial contractility
- sympathetic overactivity
- resistance to the effects of catecholamines
- peripheral arteriolar vasodilatation
- venoconstriction of peripheral veins
- vasoconstriction of pulmonary arteries (increased PAP)
- effects of hyperkalaemia on heart
maintenance of cardiac output and SVR due to catecholamine release while plasma pH remains above 7.2.
- increased bone resorption (chronic acidosis only)
- shift of K+ out of cells causing hyperkalaemia
- a metabolic acidosis is often strongly suspected because of the clinical presentation of the patient (eg diabetes, renal failure, severe diarrhoea).
- 3 clues from a typical hospital automated biochemical profile are:
- (i) low ‘bicarbonate’ (or low ‘total CO2’)
- (ii) high chloride
- (iii) high anion gap
other useful investigations:
- (i) urine tests for glucose and ketones
- (ii) electrolytes (incl chloride, anion gap, ‘bicarbonate’)
- (iii) plasma glucose
- (iv) urea and creatinine
- (v) lactate
useful additional indices in assessment of metabolic acidosis include:
- (i) Anion gap
- (ii) Delta ratio
- (iii) Urinary anion gap
- (iv) Osmolar gap
- compensation = hyperventilation to decrease the arterial pCO2.
- detected by both the peripheral and central chemoreceptors and the respiratory center
- maximal compensation takes 12 to 24 hours
- the last two digits of pH should approximately equal the PaCO2 (works well for pH between 7.10-7.60)
Expected pCO2 = 1.5 (Actual [HCO3] ) + 8 mmHg
- the limiting value of compensation is the lowest level to which the pCO2 can fall – this is typically 8 to 10mmHg, though lower values are occasionally seen.
- if a patient with a severe metabolic acidosis requires intubation -> hyperventilate otherwise acidosis will worsen
- carbon dioxide crosses cell membranes readily so intracellular pH falls rapidly also, resulting in depression of myocardial contractility, arrhythmias and a rise in intracranial pressure.
- find cause and treat
- provide supportive treatment (eg fluids, oxygen, treatment for hyperkalaemia)
- in most cases, IV sodium bicarbonate is NOT necessary, NOT helpful, & may even be harmful in the treatment of metabolic acidosis.
- renal generation of new bicarbonate -> this usually occurs as a consequence of an increase in ammonium excretion.
- hepatic metabolism of acid anions to produce bicarbonate -> the normal liver has a large capacity to metabolise many organic acid anions (eg lactate, ketoanions) with the result that bicarbonate is regenerated in the liver
- in DKA ketoacids are lost in diuresis thus aren’t available for HCO3 regeneration
Exogenous Administration of sodium bicarbonate
- time honoured method to ‘speed up’ the return of bicarbonate levels to normal.
- may be useful in mineral acidosis (hyperchloraemic metabolic acidosis) where there are no endogenous acid anions which can be metabolised by the liver.
- in most other cases of metabolic acidosis this administration is either not helpful or may be disadvantageous.
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.