Q4
LONG ANSWER
10M
★ High-yield
Classify the acid–base disorders. Describe their causes, compensation and the use of the anion gap.
Normal Values
| Parameter | Normal range |
|---|---|
| Arterial pH | 7.35–7.45 |
| PCO2 | 35–45 mmHg |
| HCO3− | 22–26 mEq/L |
| PO2 | 80–100 mmHg |
| Base excess | −2 to +2 mEq/L |
| Anion gap | 8–16 mEq/L |
Henderson–Hasselbalch: pH = 6.1 + log ([HCO3−] ÷ 0.03 × pCO2)The ratio of bicarbonate to carbonic acid is normally 20 : 1.
- The kidney controls the numerator (bicarbonate); the lung controls the denominator (pCO2). Every acid–base disorder is a disturbance of one, compensated by the other
The Four Primary Disorders
| Disorder | Primary change | PH | Compensation | Speed |
|---|---|---|---|---|
| Metabolic acidosis | ↓ HCO3 | ↓ | ↓ pCO2 (hyperventilation) | Minutes to hours |
| Metabolic alkalosis | ↑ HCO3 | ↑ | ↑ pCO2 (hypoventilation) | Hours; limited |
| Respiratory acidosis | ↑ pCO2 | ↓ | ↑ HCO3 (renal) | Days |
| Respiratory alkalosis | ↓ pCO2 | ↑ | ↓ HCO3 (renal) | Days |
- Compensation never fully corrects the pH — if the pH is normal with abnormal values, suspect a mixed disorder
- Respiratory compensation is fast; renal compensation is slow but far more powerful
Metabolic Acidosis and the Anion Gap
Anion gap = Na+ − (Cl− + HCO3−); normal 8–16 mEq/L. It represents the unmeasured anions, chiefly albumin.
| High anion gap (added acid) | Normal anion gap (bicarbonate lost) |
|---|---|
| Methanol | Diarrhoea — the commonest |
| Uraemia | Renal tubular acidosis |
| Diabetic ketoacidosis | Pancreatic or biliary fistula |
| Paraldehyde | Acetazolamide |
| Isoniazid, Iron | Ureteric diversion |
| Lactic acidosis | Excess saline (hyperchloraemic) |
| Ethylene glycol | — |
| Salicylates | — |
- Mnemonic mudpiles for the raised gap causes
- Normal anion gap acidosis is also called hyperchloraemic — chloride rises to replace the lost bicarbonate
- The gap must be corrected for albumin — add 2.5 mEq/L for every 1 g/dL that albumin falls below 4
Causes of the Other Disorders
| Disorder | Causes |
|---|---|
| Metabolic alkalosis | Vomiting, nasogastric suction, diuretics, hyperaldosteronism, excess alkali, hypokalaemia |
| Respiratory acidosis | COPD, respiratory depression (opioids, anaesthesia), neuromuscular disease, airway obstruction, severe asthma |
| Respiratory alkalosis | Anxiety and hyperventilation, high altitude, fever, sepsis, early salicylate poisoning, hepatic failure, pregnancy |
Approach to Interpretation
- 1. Look at the pH — acidaemia or alkalaemia? → 2.
- Which value explains it — HCO3 (metabolic) or pCO2 (respiratory)? → 3.
- Is compensation appropriate? Use the expected formulas → 4.
- If metabolic acidosis, calculate the anion gap → 5.
- If the gap is raised, check the delta ratio for a second disorder → 6.
- Interpret alongside the clinical picture
- Winter formula for metabolic acidosis: expected pCO2 = 1.5 × HCO3 + 8 ± 2. A higher value means a coexisting respiratory acidosis; a lower one, a respiratory alkalosis
Clinical Consequences
- Acidosis — Kussmaul breathing, reduced myocardial contractility, vasodilatation, arrhythmias, hyperkalaemia, insulin resistance, confusion
- Alkalosis — tetany (ionised calcium falls), paraesthesiae, confusion, hypokalaemia, arrhythmias; the oxygen dissociation curve shifts left
- Acidosis raises serum potassium by shifting it out of cells; alkalosis lowers it — a link that must be remembered when correcting either
Compensation Formulas
| Primary disorder | Expected compensation |
|---|---|
| Metabolic acidosis | PCO2 = 1.5 × HCO3 + 8 ± 2 (Winter) |
| Metabolic alkalosis | PCO2 rises 0.7 mmHg per 1 mEq/L rise in HCO3 |
| Acute respiratory acidosis | HCO3 rises 1 mEq/L per 10 mmHg rise in pCO2 |
| Chronic respiratory acidosis | HCO3 rises 3.5 mEq/L per 10 mmHg |
| Acute respiratory alkalosis | HCO3 falls 2 mEq/L per 10 mmHg fall |
| Chronic respiratory alkalosis | HCO3 falls 5 mEq/L per 10 mmHg fall |
Applied Aspects
- Salicylate poisoning gives a mixed picture — direct stimulation of the respiratory centre causes respiratory alkalosis, while uncoupling and lactate cause metabolic acidosis. A normal pH here is ominous
- Treat the cause, not the number — bicarbonate in lactic acidosis and DKA is reserved for severe acidaemia, and may worsen intracellular pH
- Correcting acidosis unmasks hypokalaemia and can precipitate arrhythmia; potassium must be replaced alongside
- In chronic COPD the bicarbonate is high from renal compensation; giving too much oxygen removes the hypoxic drive and worsens CO2 retention
- Venous blood gases suffice for pH and bicarbonate in most non-respiratory situations, sparing an arterial puncture
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