Pathophysiology
P-II-18. Acid-base disorder, Case 1
酸塩基平衡障害 症例1
Case Presentation
A 35-year-old woman with asthma presents to the clinic. She says she has had frequent diarrhea for the last three months. She has also had a fever (39°C) in the last few days.
Physical examination: Patient is a well-developed, thin woman, moderately agitated.
Vital signs:
- Blood pressure 100/60 mmHg (supine), pulse 100/min
- Blood pressure 80/40 mmHg (standing), pulse 125/min
- Respiratory rate 18/min
Examination findings:
- Lungs: expiration prolonged, slight wheezing sound at the end
- Abdomen flexible and minimally tender to palpation
- Bowel sounds suggest a markedly hyperactive bowel movement
- Stools negative for blood
- No cyanosis or edema
Laboratory Values
Arterial blood gas:
- pH 7.31
- PCO₂ 32 mmHg
- PO₂ 90 mmHg
- Bicarbonate 12 mmol/l
Chemistry (value / normal range):
- Sodium 136 (135–146 mmol/l)
- Potassium 3.4 (3.5–5.1 mmol/l)
- Chloride 112 (98–107 mmol/l)
- Calcium 2.32 (2.2–2.65 mmol/l)
- BUN 8 (2.8–7.2 mmol/l)
- Creatinine 85 (45–84 µmol/l)
- Glucose 4.5 (3.9–5.8 mmol/l)
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| pH 7.31; HCO₃ 12 mmol/l (low) | Acidaemia with low bicarbonate → metabolic acidosis |
| PCO₂ 32 mmHg (low) | Appropriate respiratory compensation (hyperventilation blows off CO₂) |
| Anion gap = 136 − (112 + 12) = 12; chloride 112 (high) | Normal anion gap, hyperchloraemic metabolic acidosis |
| “frequent diarrhea for the last three months”; hyperactive bowel sounds | Gastrointestinal loss of bicarbonate → the cause of the acidosis |
| Potassium 3.4 (low) | Potassium also lost in diarrhoea → hypokalaemia |
| BP 100/60 supine → 80/40 standing; pulse 100→125 | Orthostatic hypotension/tachycardia → volume depletion from fluid loss |
| Stools negative for blood | Non-inflammatory (secretory) diarrhoea rather than a bloody colitis |
Key Points
- Diagnosis: Normal anion gap (hyperchloraemic) metabolic acidosis due to chronic diarrhoea.
- Compensation: Low PCO2 shows appropriate respiratory compensation.
- Mechanism: Loss of bicarbonate-rich intestinal fluid → the kidney retains chloride to maintain electroneutrality → normal anion gap.
- Associated losses: Hypokalaemia and volume depletion (orthostatic vital signs) from ongoing diarrhoea.
- Contrast: Differs from high-anion-gap acidosis (e.g., ketoacidosis), where unmeasured acids accumulate.
一問一答
▶What is the acid-base diagnosis in a patient with chronic diarrhoea, pH 7.31, HCO3 12, and a normal anion gap?
Normal anion gap (hyperchloraemic) metabolic acidosis.
▶How is the anion gap calculated, and what is it here?
Anion gap = Na − (Cl + HCO3) = 136 − (112 + 12) = 12, which is normal.
▶Why does chronic diarrhoea cause a normal anion gap metabolic acidosis?
Loss of bicarbonate-rich intestinal fluid lowers HCO3; the kidney retains chloride for electroneutrality, keeping the gap normal.
▶What does a low PCO2 (32 mmHg) signify in this metabolic acidosis?
Appropriate respiratory compensation — hyperventilation lowers CO2 to limit the fall in pH.
▶Why is the chloride elevated (112) in this patient?
The kidney retains chloride to replace lost bicarbonate, producing hyperchloraemia.
▶Why is potassium low (3.4) in chronic diarrhoea?
Potassium is lost in the diarrhoeal fluid, causing hypokalaemia.
▶What do orthostatic vital signs (BP 100/60 supine → 80/40 standing, pulse 100→125) indicate?
Volume depletion from ongoing fluid loss in diarrhoea.
▶What does the anion gap represent physiologically?
Unmeasured anions in plasma; an increase reflects accumulation of acids like lactate or ketones.
▶What are common causes of a normal anion gap metabolic acidosis?
Diarrhoea (GI bicarbonate loss) and renal tubular acidosis.
▶Why are the stools negative for blood relevant here?
It suggests a non-inflammatory (secretory) diarrhoea rather than a bloody colitis.
▶What is the expected respiratory compensation in metabolic acidosis (Winter's formula)?
Expected PCO2 ≈ 1.5 × HCO3 + 8 (±2); deviation indicates an additional respiratory disorder.
▶What is the mainstay of treatment for diarrhoeal metabolic acidosis?
Fluid and electrolyte (including bicarbonate/potassium) replacement and treating the underlying cause.
▶Why can severe acidosis impair cardiovascular function?
Low pH reduces myocardial contractility and the vascular response to catecholamines.
▶How does acidaemia affect the potassium balance in general?
Acidaemia tends to shift potassium out of cells (raising serum K), though total-body K may be depleted as in this diarrhoea case.
▶Why is the slightly raised creatinine/BUN consistent with this picture?
Volume depletion causes pre-renal impairment of kidney perfusion.
▶What is the role of bicarbonate as the body's main buffer?
Bicarbonate neutralizes excess hydrogen ions; its loss/consumption leads to metabolic acidosis.
▶Why does compensation by the lungs occur quickly while renal compensation is slow?
Ventilation adjusts CO2 within minutes, whereas renal bicarbonate handling takes hours to days.
▶How does respiratory compensation never fully correct the pH?
Compensation only buffers the change; the pH stays on the acidic side unless the primary disorder is corrected.
▶Why is hypokalaemia dangerous in this patient?
It can cause muscle weakness and cardiac arrhythmias.
▶How does this diarrhoeal acidosis differ from high-anion-gap acidosis?
Here bicarbonate is lost with chloride retention (normal gap), whereas high-gap acidosis is from added unmeasured acids.