Metabolic Acidosis

OVERVIEW

• 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

CAUSES

• 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).

CLASSIFICATION

High anion gap (HAGMA)

• Lactate
• Toxins – methanol, metformin, phenformin, paraldehyde, propylene glycol, pyroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salicylates, solvents
• Ketones
• Renal

Normal anion gap (NAGMA)

• Chloride
• Acetazolamide and Addisons
• GI causes – diarrhoea, vomiting, fistulas (pancreatic, ureterostomies, small bowel, ileostomies)
• Extras – RTA

MAINTENANCE

• 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.

EFFECTS

Respiratory Effects

• 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.

Cardiovascular Effects

• 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.

Other effects

• increased bone resorption (chronic acidosis only)
• shift of K+ out of cells causing hyperkalaemia

ASSESSMENT

• 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

• 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.

CORRECTION

• 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.

• Kidney:
  • renal generation of new bicarbonate -> this usually occurs as a consequence of an increase in ammonium excretion.
• Liver:
  • 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