Acid-Base abnorrmalities

Related Subjects: |Metabolic acidosis |Aspirin or Salicylates toxicity |Ethylene glycol toxicity |Renal Tubular Acidosis |Lactic acidosis |Metabolic alkalosis

🧪 Acid–base disturbances are common in acute medicine and exams because they reveal what the body is doing: ventilation (lungs), buffering/renal handling (kidneys), and the underlying pathology (sepsis, DKA, COPD, vomiting, toxins). A safe approach is always the same: check pH → decide primary process → check compensation → calculate anion gap → hunt for mixed disorders → treat the cause.

🔑 Key definitions

• Acidaemia = pH < 7.35 (blood is acidic). Alkalaemia = pH > 7.45.
• Acidosis / alkalosis = the process driving pH down/up (you can have both at once).
• Respiratory disorders change PaCO₂ (ventilation). Metabolic disorders change HCO₃⁻ / base excess (kidney + buffers).
• Compensation = predictable physiological response in the opposite system (lungs compensate quickly; kidneys compensate slowly).

📌 Normal values (adult ABG)

🧭 Stepwise ABG interpretation (the Makindo method)

1. Is the sample plausible? Look at O₂ saturation vs PaO₂, and clinical context (on oxygen? COPD?).
2. Step 1 — What is the pH? Acidaemia vs alkalaemia.
3. Step 2 — What matches the pH?
   • Acidaemia + high PaCO₂ → primary respiratory acidosis
   • Acidaemia + low HCO₃⁻ / negative BE → primary metabolic acidosis
   • Alkalaemia + low PaCO₂ → primary respiratory alkalosis
   • Alkalaemia + high HCO₃⁻ / positive BE → primary metabolic alkalosis
4. Step 3 — Is compensation appropriate? If it’s too little or too much → suspect a mixed disorder.
5. Step 4 — If metabolic acidosis: calculate the anion gap and check lactate/ketones.
6. Step 5 — Treat the cause (not the number): oxygen/ventilation, fluids, insulin, antibiotics, antidotes, dialysis, etc.

🧠 Clinical pearl: “Normal pH” does not mean normal physiology. A mixed metabolic acidosis + metabolic alkalosis can give a near-normal pH while the patient is critically ill.

🫁 Respiratory disorders (PaCO₂-driven)

1) Respiratory acidosis 😮‍💨 (hypoventilation)

• Pattern: pH ↓, PaCO₂ ↑ (kPa rises), HCO₃⁻ may rise if chronic.
• Mechanism: reduced alveolar ventilation → CO₂ retention → carbonic acid ↑ → H⁺ ↑.
• Common causes (UK acute medicine):
  • Acute exacerbation of COPD (type 2 respiratory failure)
  • Severe asthma / fatigue
  • Opioids, benzodiazepines, sedatives
  • Neuromuscular weakness (GBS, myasthenia), chest wall disease
  • Severe obesity hypoventilation, sleep-related hypoventilation
• Immediate priorities: ABC approach, controlled oxygen if CO₂ retainers, reverse sedatives where appropriate, ventilatory support if tiring/acidotic.

Acute vs chronic respiratory acidosis

2) Respiratory alkalosis 😤 (hyperventilation)

• Pattern: pH ↑, PaCO₂ ↓, HCO₃⁻ may fall if chronic.
• Mechanism: increased ventilation → CO₂ washout → H⁺ falls.
• Common causes:
  • Anxiety/panic, pain
  • Sepsis (often early), fever
  • Pregnancy (progesterone-driven hyperventilation)
  • Salicylate poisoning (early respiratory alkalosis)
  • Hypoxia-driven hyperventilation: PE, pneumonia, asthma

🫀 Exam trap: A patient with PE may have respiratory alkalosis (hyperventilation) plus lactate from shock → a mixed picture.

🧫 Metabolic disorders (HCO₃⁻-driven)

3) Metabolic acidosis ☠️ (loss of base or gain of acid)

• Pattern: pH ↓, HCO₃⁻ ↓ / BE negative; compensation = PaCO₂ falls (hyperventilation, “Kussmaul”).
• Mechanism: either production/ingestion of acids (lactate, ketones, toxins) or loss of bicarbonate (GI/renal).

Step 4a: Anion gap (AG) — the must-know calculation

Anion gap estimates “unmeasured anions” in plasma.

AG = Na⁺ − (Cl⁻ + HCO₃⁻)

• Typical normal AG ≈ 8–12 mmol/L (varies by lab).
• Albumin matters: low albumin lowers the expected AG (so a “normal” AG can hide a high-gap acidosis).

Albumin-corrected anion gap (useful in sick patients)

A common correction:

Corrected AG ≈ AG + 2.5 × (40 − albumin [g/L])

High anion gap metabolic acidosis (HAGMA) 🔥

Normal anion gap metabolic acidosis (NAGMA / hyperchloraemic) 💧

🧠 Pathophysiology pearl: In NAGMA the “missing bicarbonate” is often replaced by chloride to maintain electroneutrality, hence hyperchloraemia. In HAGMA bicarbonate is consumed buffering “new acids” (lactate, ketones, toxins), leaving unmeasured anions behind.

Compensation in metabolic acidosis (does it fit?)

When metabolic acidosis is primary, the lungs compensate by lowering PaCO₂. A useful rule (Winters’ formula, mmHg) is:

Expected PaCO₂ ≈ (1.5 × HCO₃⁻) + 8 ± 2

• If measured PaCO₂ is higher than expected → additional respiratory acidosis (e.g., COPD + DKA).
• If measured PaCO₂ is lower than expected → additional respiratory alkalosis (e.g., sepsis + metabolic acidosis).

4) Metabolic alkalosis 🌪️ (gain of base or loss of acid)

• Pattern: pH ↑, HCO₃⁻ ↑ / BE positive; compensation = PaCO₂ rises (hypoventilation) but is limited by hypoxia.
• Mechanisms:
  • Loss of gastric acid: vomiting, NG suction → H⁺ loss raises HCO₃⁻
  • Diuretics: volume contraction (“contraction alkalosis”), increased distal Na delivery → H⁺/K⁺ loss
  • Mineralocorticoid excess: hyperaldosteronism → H⁺ and K⁺ wasting
• Clinical associations: hypokalaemia, hypochloraemia, volume depletion.
• Management principles: treat cause, replace chloride and volume (e.g., IV 0.9% saline if appropriate), correct K⁺ and Mg²⁺, review diuretics, consider endocrine causes if persistent.

🧠 Why hypokalaemia matters: low K⁺ drives K⁺ out of cells in exchange for H⁺ moving in → extracellular H⁺ falls → alkalosis worsens; the kidney also increases H⁺ secretion in hypokalaemia.

🧩 Mixed acid–base disorders (how to spot them) 🔍

• Red flag 1: pH near normal but HCO₃⁻ and PaCO₂ both abnormal.
• Red flag 2: Compensation “doesn’t fit” (too much or too little).
• Red flag 3: In metabolic acidosis, anion gap is high but chloride is also high → suggests mixed HAGMA + NAGMA.
• Common mixed patterns:
  • Sepsis: respiratory alkalosis (hyperventilation) + lactic acidosis
  • DKA + vomiting: metabolic acidosis + metabolic alkalosis (pH may be normal-ish)
  • COPD exacerbation + sepsis: respiratory acidosis + lactic acidosis
  • Salicylates: early respiratory alkalosis + later high anion gap acidosis

🚑 Practical clinical approach (UK ward/ED)

1. Assess the patient first: airway, work of breathing, circulation, GCS, urine output.
2. Look at lactate (shock/sepsis), glucose + ketones (DKA), U&E (renal failure, K⁺), and medication/toxin history.
3. Severe acidaemia (e.g., pH < 7.1) is dangerous: impaired myocardial contractility, arrhythmia risk, catecholamine resistance → treat the cause urgently and involve seniors/ICU early.
4. Ventilation failure with rising CO₂ and falling pH: consider NIV/intubation depending on cause, trajectory, and ceilings of care.
5. Bicarbonate therapy is not routine for most metabolic acidosis; it may be considered in selected cases (e.g., certain severe acidaemia with haemodynamic compromise, or specific poisonings/RTAs) but the priority is always fixing the underlying driver.

🧠 Worked patterns (exam-style mini cases)

Case 1: DKA 🍬

• pH 7.12, HCO₃⁻ 8, PaCO₂ low, ketones high, glucose high
• Diagnosis: primary metabolic acidosis (high AG) with respiratory compensation (Kussmaul)
• Action: DKA protocol: fluids, insulin, K⁺, close monitoring

Case 2: COPD exacerbation 😮‍💨

• pH 7.28, PaCO₂ 9.0 kPa, HCO₃⁻ 30
• Diagnosis: respiratory acidosis with metabolic (renal) compensation (chronic component)
• Action: controlled O₂, bronchodilators, steroids/antibiotics if indicated, consider NIV if persistent acidosis

Case 3: Vomiting + diuretics 🌪️

• pH 7.52, HCO₃⁻ 34, PaCO₂ mildly raised, K⁺ low, Cl⁻ low
• Diagnosis: metabolic alkalosis with partial respiratory compensation
• Action: correct volume/K⁺/Cl⁻, review diuretics, treat vomiting

🧰 Quick reference summary table

✅ Makindo exam tip: Always state (1) primary disorder, (2) whether compensation is appropriate, (3) likely cause, and (4) immediate management priority. That structure scores marks and mirrors real-life clinical reasoning.