metabolic acidosis

introduction

a primary metabolic acidosis is a derangement of normal physiology characterised by a low arterial pH and a low arterial bicarbonate level.
if arterial bicarbonate level is low but pH is high, then this is a compensatory metabolic acidosis which is the body's attempt to correct a prolonged primary respiratory alkalosis event - see acid-base physiology
there are many possible causes of a primary metabolic acidosis, and we often resort to looking at the anion gap as a starting point to determining the main cause.

this is associated with hyperchloraemia and is due to either loss of bicarbonate or excessive intake of proton donors
it may also occur excessive dilution with rapid extracellular fluid expansion

diarrhoea;
small bowel, biliary, or pancreatic tube or fistula drain;
ureteral diversion with bowel (ileal conduit):
bowel augmentation cystoplasty;
exogenous chloride intake: CaCl2, MgCl2, NH4Cl, cholestyramine, HCl, arginine HCl;
impaired urinary acidifying capacity:
- carbonic anhydrase inhibitors;
- type I renal tubular acidosis (RTA) (urinary pH > 5.3 eg. obstructive uropathy, nephrocalcinosis, lithium, toluene)
- type II renal tubular acidosis (RTA) (urinary pH acidic thus less severe acidosis eg. Fanconi syndrome, lead, myeloma, amyloid)

type IV renal tubular acidosis (RTA):
- mineralocorticoid deficiency (look for intravascular volume depletion and urinary Na > 10mmol/L)
- eg. diabetic nephropathy, ch. pyelonephritis, ch. urinary obstruction, aldosterone antagonists (mineralocorticoid receptor antagonists (MRAs) )
sulphur intoxication

shock - hypovoalemic/cardiogenic/septic;
severe hypoxia
severe anaemia
severe asthma ⇒ work of breathing increased
- ⇒ decreased preload due to increased i/thoracic pressure
seizures (takes >1hr to be metabolised back to normal)
severe exercise
cyanide poisoning poisoning