| Mechanism |
| Primary disturbance | ↓HCO₃⁻ from added acid (AG expanded) | ↓HCO₃⁻ with Cl⁻ gain (AG normal) | ↑PaCO₂ (alveolar hypoventilation) | ↓PaCO₂ (hyperventilation) |
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| Assessment |
| Expected compensation | Winter: expected PaCO₂ ≈ 1.5×HCO₃⁻ + 8 (±2) | Same Winter relation applies | Acute: HCO₃⁻ +1 per 10 mmHg PaCO₂; Chronic: +3.5–4 per 10 | Acute: HCO₃⁻ −2 per 10; Chronic: −4–5 per 10 |
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| Traps & pitfalls |
| Common ICU causes | Lactic (shock, metformin), ketoacidosis (DM/alcohol), toxins (methanol, ethylene glycol, salicylate), renal failure | GI HCO₃⁻ loss (diarrhea, fistula/high-output stoma), RTAs, acetazolamide, large-volume saline (hyperchloremic) | Sedatives/opioids, neuromuscular weakness (GBS/MG/high cord), COPD exacerbation, obesity hypoventilation, fatigue/auto-PEEP in late ARDS | Pain/anxiety, hypoxemia, early sepsis, PE, liver failure, salicylates, over-ventilation |
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| Assessment |
| Key calculations | AG = Na − (Cl + HCO₃⁻); ΔΔ gap to expose a second (normal-AG) disorder; osmolar gap if toxin suspected; correct AG for albumin (+~2.5 per 1 g/dL below 4) | Urine anion gap; ΔΔ (low ratio suggests combined HAGMA+NAGMA) | Compare measured HCO₃⁻ vs expected → exposes superimposed metabolic disorder | Same expected-compensation comparison |
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| Traps & pitfalls |
| Common traps | Hypoalbuminemia masks a high AG; D-lactate not detected on standard lactate assay | Post-saline acidosis misread as worsening AKI acidosis | Rising post-intubation PaCO₂ from AUTO-PEEP mistaken for worsening disease | Near-normal pH from mixed disturbances hides severity; severe alkalemia → arrhythmia, ↓cerebral flow, ↓ionized Ca²⁺ |
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