Acute renal and fluid problems

Acid–base disorders

Overview and approach

Classify metabolic versus respiratory disorders and look for mixed disturbances.

  • Stepwise: is the pH acidaemic (below 7.35) or alkalaemic (above 7.45)? Do PCO2 and pH move in opposite directions (respiratory) or the same direction (metabolic)? Is compensation appropriate? Calculate the anion gap in metabolic acidosis1.
  • See the Blood gas interpretation (ABG/VBG) page for the detailed table and causes.
  • How metabolic acidosis arises: extra acid (lactate, ketones, toxins), loss of bicarbonate (diarrhoea, small bowel drainage) or failure to excrete acid (kidney failure)3.
  • Metabolic alkalosis needs two steps: something generates it (usually acid loss from vomiting, or alkali intake), and something stops the kidney excreting the extra bicarbonate. The usual maintainers are volume, chloride and potassium depletion, or autonomous aldosterone excess3.
  • In CKD: acidosis is usually normal anion gap while GFR is roughly 20-50, and becomes high anion gap once GFR falls below about 20, as ammonia production falls with nephron loss3.
Assessment and clinical features

Clinical context, ventilation, perfusion, GI loss, renal disease, diabetes and toxins.

  • Match the gas to the patient: respiratory rate and effort, perfusion, vomiting or diarrhoea, diuretics, kidney disease, diabetes and ketones, ingestions.
  • What acidaemia does: deep, sighing (Kussmaul) breathing; reduced cardiac contractility (partly masked by catecholamines); venoconstriction that makes pulmonary oedema likely with little extra fluid; headache, drowsiness through to coma; and glucose intolerance3.
  • Metabolic alkalosis clues: alkalosis with hypertension and hypokalaemia suggests mineralocorticoid excess or diuretic use; with normal BP and hypokalaemia think vomiting (including hidden), diuretics, Bartter or Gitelman syndrome, or magnesium deficiency3.
  • Salicylate poisoning typically gives a respiratory alkalosis, often mixed with a high anion gap metabolic acidosis3.
  • CKD with metabolic acidosis is common; bicarbonate and eGFR trends matter2.
Differentials and investigations

Interpret pH, CO2 and bicarbonate with compensation and anion gap; assess albumin and lactate/ketones when relevant.

  • Metabolic acidosis: HCO3 low, compensatory CO2 fall. Metabolic alkalosis: HCO3 high, CO2 rises. Respiratory acidosis: CO2 high, HCO3 rises. Respiratory alkalosis: CO2 low, HCO3 falls1.
  • Anion gap = Na minus (Cl + HCO3), about 8 to 12 without potassium; correct for albumin. Raised gap: uraemia, DKA, lactic acidosis, toxic alcohols, salicylate. Normal gap: diarrhoea, renal tubular acidosis, acetazolamide1. Reference ranges vary by laboratory.
  • Expected compensation (outside these ranges, suspect a second disorder)3.
Primary disorderExpected response
Metabolic acidosisPaCO2 about 1.5 x HCO3 + 8 (plus or minus 2)
Metabolic alkalosisPaCO2 rises about 0.75 mmHg per 1 mmol/L rise in HCO3
Respiratory acidosisHCO3 rises 1 per 10 mmHg CO2 rise (acute), 4 per 10 (chronic)
Respiratory alkalosisHCO3 falls 2 per 10 mmHg CO2 fall (acute), 4 per 10 (chronic)
  • Delta check: in a high anion gap acidosis compare the rise in anion gap with the fall in bicarbonate. A gap rise much bigger than the bicarbonate fall means a coexisting metabolic alkalosis (e.g. uraemia with vomiting); a bicarbonate fall much bigger than the gap rise means an added normal-gap acidosis3.
  • Albumin and the gap: each 10 g/L fall in albumin lowers the anion gap by about 2.5. A low gap also occurs with myeloma paraproteins and lithium toxicity3.
  • The four high-gap groups: lactic acidosis, ketoacidosis (diabetic, alcoholic, starvation), toxins (methanol, ethylene glycol, salicylate, propylene glycol, pyroglutamic acid from paracetamol in the critically ill) and kidney failure3.
  • Lactic acidosis: type A from poor perfusion or oxygen delivery (shock, severe anaemia, carbon monoxide, cyanide); type B without hypoperfusion (metformin, liver failure, malignancy, thiamine deficiency, seizures). In a sick vasculopath on vasopressors, think of hidden bowel ischaemia3.
  • Osmolar gap: measured minus calculated osmolality above about 15-20 suggests an extra solute. Methanol and ethylene glycol raise both the osmolar and anion gaps; isopropyl alcohol raises only the osmolar gap. Oxalate crystals in urine point to ethylene glycol3.
  • Urine anion gap (urine Na + K minus Cl) in normal-gap acidosis: negative means the kidney is excreting ammonium appropriately, so the loss is from the gut; positive suggests renal tubular acidosis3.
  • Urine ketone dipsticks detect acetoacetate, not beta-hydroxybutyrate. They can underestimate ketosis in alcoholic ketoacidosis and may look more positive as the patient improves3.
  • Urine chloride in metabolic alkalosis: low urine chloride suggests vomiting or past diuretic use; urinary chloride loss with hypokalaemia suggests current diuretics, Bartter or Gitelman syndrome, or mineralocorticoid excess3.
  • The bicarbonate calculated on the blood gas and the measured value on the electrolyte panel should agree within about 2 mmol/L; if not, suspect a sampling or lab error3.
  • Metabolic alkalosis: vomiting, diuretics, heart failure, renal artery stenosis1.
  • A venous gas does not reliably assess arterial oxygenation.
Management and follow-up

Treat the underlying cause rather than a blood-gas number; severe disorders need monitored expert care.

  • Treat the cause (sepsis, DKA, hypoperfusion, respiratory failure, toxin). Bicarbonate therapy is selective and specialist-guided.
Red flags and clinical pearls

A near-normal pH may hide a mixed dangerous disorder. VBG does not reliably replace arterial oxygen assessment.

  • Acidaemia and alkalaemia refer to pH; acidosis and alkalosis refer to the process.
  • Normal pH with abnormal CO2 and HCO3 suggests a mixed disorder.
  • A raised anion gap means an anion gap acidosis is present even when the pH and bicarbonate look normal3.
  • Dangerous mixes: a patient with COPD may not be able to blow off CO2 to compensate for a metabolic acidosis, so the pH falls steeply. Alcoholic ketoacidosis often combines ketoacidosis, vomiting-related alkalosis and respiratory alkalosis3.
References
  1. StatPearls: Anion Gap and Non-Anion Gap Metabolic Acidosis (as cited on the Blood gas page)
  2. Kidney Health Australia: CKD Management in Primary Care handbook
  3. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. Chapter 47, Acidosis and alkalosis.

Last updated from Sen’s notes on 22 October 2026.