Pathophysiology
P-II-21. Acid-base disorder, Case 4
酸塩基平衡障害 症例4
Case Presentation
The ambulance brings to the hospital a 75-year-old man with a long history of chronic obstructive pulmonary disease, which often leads to acute exacerbations. The patient presents with fever, confusion and severe dyspnea. He lives alone but his neighbor says he has been ill for a week and his condition has worsened in the last 4 days. He has been smoking 2 packs a day for decades.
Laboratory Values
Arterial blood gas:
- pH 7.13
- PCO₂ 70 mmHg
- PO₂ 65 mmHg
- Bicarbonate 9 mmol/l
Chemistry (value / normal range):
- Sodium 145 (135–146 mmol/l)
- Potassium 6.5 (3.5–5.1 mmol/l)
- Chloride 110 (98–107 mmol/l)
- Calcium 2.2 (2.2–2.65 mmol/l)
- BUN 7.5 (2.8–7.2 mmol/l)
- Creatinine 80 (45–84 µmol/l)
- Glucose 6.5 (3.9–5.8 mmol/l)
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| pH 7.13 (severe acidaemia) | Life-threatening acidosis |
| PCO₂ 70 mmHg (high) | Respiratory acidosis — CO₂ retention from COPD/hypoventilation |
| HCO₃ 9 mmol/l (very low) | A coexisting metabolic acidosis (bicarbonate is consumed, not raised as compensation would predict) |
| Anion gap = 145 − (110 + 9) = 26 (high) | High anion gap metabolic acidosis — likely lactic acidosis from hypoxaemia/sepsis |
| Low pH with BOTH high PCO₂ and low HCO₃ | A mixed disorder — the two acidoses add together (no adequate compensation in either direction) |
| “fever, confusion and severe dyspnea”; ill for a week | Severe infection (pneumonia/sepsis) driving the metabolic (lactic) component |
| Potassium 6.5 mmol/l (high); PO₂ 65 mmHg | Hyperkalaemia (acidosis shifts K⁺ out of cells) and hypoxaemia |
Key Points
- Diagnosis: Mixed acid-base disorder — respiratory acidosis (COPD/CO₂ retention) PLUS a high anion gap metabolic acidosis (lactic acidosis from sepsis/hypoxaemia).
- How to recognise it: A severely low pH with simultaneously high PCO2 and low HCO3 — both primary acidoses, not compensation.
- Mechanism: Failing ventilation retains CO2, while tissue hypoxia/sepsis generates lactic acid → the disturbances compound each other.
- Severity: pH 7.13 with hyperkalaemia is a medical emergency.
- Contrast: Differs from a simple respiratory acidosis, where bicarbonate would be high (compensatory), not low.
一問一答
▶What is the acid-base diagnosis in a COPD patient with pH 7.13, PCO2 70, and HCO3 9?
A mixed disorder: respiratory acidosis plus a high anion gap metabolic acidosis.
▶How do you recognise a mixed acidosis from the blood gas here?
A severely low pH with simultaneously high PCO2 AND low HCO3 — both are primary acidoses, not compensation.
▶Why is the high PCO2 (70) evidence of respiratory acidosis here?
Failing ventilation in COPD retains CO2, lowering pH.
▶Why does the very low bicarbonate (9) indicate a coexisting metabolic acidosis?
In a pure respiratory acidosis bicarbonate would rise as compensation; a low value means bicarbonate is being consumed by a metabolic acidosis.
▶What is the anion gap here, and what is the likely metabolic cause?
AG = 145 − (110 + 9) = 26 (high); likely lactic acidosis from hypoxaemia/sepsis.
▶What is the likely source of the lactic acidosis in this patient?
Severe infection (pneumonia/sepsis) with tissue hypoperfusion and hypoxaemia.
▶Why is hyperkalaemia (6.5) present in this acidosis?
Acidaemia shifts potassium out of cells into the blood.
▶Why is a pH of 7.13 a medical emergency?
Severe acidaemia depresses cardiac contractility and can cause life-threatening arrhythmias, especially with hyperkalaemia.
▶What is lactic acidosis and how is it generated?
A high anion gap acidosis from anaerobic metabolism producing lactic acid when tissue oxygen delivery is inadequate.
▶How does this mixed picture differ from a simple (chronic) respiratory acidosis?
In simple respiratory acidosis bicarbonate is high (renal compensation); here it is low because of the added metabolic acidosis.
▶Why does COPD cause CO2 retention?
Severe airflow obstruction and alveolar hypoventilation impair CO2 elimination.
▶Why does this patient have confusion?
Hypercapnia (CO2 narcosis), hypoxaemia, acidosis, and sepsis all impair cerebral function.
▶What is the key treatment for the respiratory component of this acidosis?
Improving ventilation (e.g. non-invasive or invasive ventilation) to clear CO2, plus treating the COPD exacerbation.
▶What treats the metabolic (lactic) component of this acidosis?
Restoring tissue perfusion and oxygenation and treating the underlying sepsis/infection.
▶How does acute respiratory acidosis differ from chronic in terms of compensation?
Acute has minimal bicarbonate rise; chronic shows significant renal bicarbonate retention over days.
▶Why must oxygen therapy be carefully titrated in this CO2-retaining patient?
Excess oxygen can worsen hypercapnia and acidosis by reducing respiratory drive and increasing V/Q mismatch.
▶Why does hyperkalaemia need urgent attention in this patient?
Combined with severe acidosis it markedly raises the risk of fatal cardiac arrhythmia.
▶How does pH determine whether a mixed disorder is dominated by acidosis or alkalosis?
The actual pH reflects the net effect; here the very low pH shows the acidoses dominate without offsetting alkalosis.
▶Why do two acidoses 'compound' rather than cancel out?
Both push pH in the same (acidic) direction, so their effects add together producing severe acidaemia.
▶Why does severe infection contribute to respiratory failure in a COPD patient?
Increased CO2 production, fatigue, and worsening gas exchange overwhelm the already-limited ventilatory reserve.