- 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