Metabolic Acid-Base Basics - The pH Tango
- Primary disturbance: Change in serum bicarbonate (HCO₃⁻).
- Metabolic Acidosis: ↓ HCO₃⁻
- Metabolic Alkalosis: ↑ HCO₃⁻
- Normal HCO₃⁻: 22-26 mEq/L.
- Normal blood pH: 7.35-7.45.
- Compensation: Respiratory system alters PaCO₂.
- Acidosis: ↓ PaCO₂ (hyperventilation)
- Alkalosis: ↑ PaCO₂ (hypoventilation)
⭐ Respiratory compensation for metabolic disorders starts within minutes but takes 12-24 hours to become maximal, while renal compensation for respiratory disorders takes 3-5 days.
Metabolic Acidosis - Sour Grapes
- Primary ↓ in serum $HCO_3^-$, leading to ↓ pH.
- Compensation: Hyperventilation (↓ PaCO₂).
- Diagnostic Flow:
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Anion Gap (AG) = $Na^+ - (Cl^- + HCO_3^-)$. Normal AG: 8-12 mEq/L.
-
Types & Causes:
Category Mnemonic Key Causes High Anion Gap (HAGMA) 📌 GOLDMARK / MUDPILES Glycols (ethylene, propylene), Oxoproline (paracetamol), L-Lactate (sepsis, shock), D-Lactate (gut malabsorption), Methanol, Aspirin (salicylates), Renal failure (uremia), Ketoacidosis (diabetic, alcoholic, starvation) Normal Anion Gap (NAGMA) / Hyperchloremic 📌 HARDUP Hyperalimentation / Hyperchloremia, Acetazolamide / Addison's disease, Renal Tubular Acidosis (RTA), Diarrhea (most common cause), Ureteroenteric fistula / Ureteral diversion, Pancreatic fistula / Parenteral nutrition
⭐ Kussmaul breathing (deep, rapid respirations) is a characteristic compensatory response to severe metabolic acidosis, aimed at blowing off CO₂.
Metabolic Alkalosis - Base Camp
- Profile: ↑ pH, ↑ HCO₃⁻.
- Pathophysiology:
- Generation: H⁺ loss (GI/renal) or HCO₃⁻ gain.
- Maintenance: Impaired renal HCO₃⁻ excretion (Cl⁻/K⁺ depletion, ↓ GFR).
- Compensation: Hypoventilation → ↑ PaCO₂.
- Expected PaCO₂ = $0.7 \times \Delta HCO_3^- + 40 \pm 2$ mmHg.
- Treatment: Saline-responsive with NaCl; Saline-resistant targets cause (e.g., K⁺ repletion, aldosterone antagonists).
Key Causes:
| Saline-Responsive (UCl⁻ < 15 mEq/L) | Saline-Resistant (UCl⁻ > 20 mEq/L) |
|---|---|
| * Vomiting/NG suction | * Hyperaldosteronism (Conn's) |
| * Diuretics (loop/thiazide) - early | * Cushing's syndrome |
| * Post-hypercapnia | * Bartter/Gitelman syndrome |
| * Villous adenoma | * Severe K⁺ depletion, Licorice |
Diagnostic Toolkit & Formulas - pH Sleuth Kit
- Anion Gap (AG): $AG = [Na^+] - ([Cl^-] + [HCO_3^-])$. Normal: 8-12 mEq/L. Detects unmeasured anions.
- Winter's Formula (Metabolic Acidosis):
⭐ Winter's formula ($Expected PaCO_2 = 1.5 imes [HCO_3^-] + 8 ext{ extpm } 2$) is crucial for assessing the appropriateness of respiratory compensation in metabolic acidosis.
- Metabolic Alkalosis $PaCO_2$ Response: $Expected PaCO_2 = (0.7 \times [HCO_3^-]) + 20 \pm 5$. Assesses respiratory compensation.
- Delta Gap ($ΔAG / ΔHCO_3^-$): For HAGMA. Ratio: $(AG_{measured} - 12) / (24 - [HCO_3^-]_{measured})$.
- Interpretation: <1 (HAGMA + NAGMA); 1-2 (Pure HAGMA); >2 (HAGMA + Met. Alkalosis).
High‑Yield Points - ⚡ Biggest Takeaways
- Metabolic Acidosis: Primary ↓ HCO3-; compensatory ↓ PCO2.
- Anion Gap (AG) is key: High AG (e.g., DKA, Lactic Acidosis) vs Normal AG (e.g., Diarrhea, RTA).
- Winter's formula predicts PCO2: (1.5 * HCO3-) + 8 ± 2.
- Metabolic Alkalosis: Primary ↑ HCO3-; compensatory ↑ PCO2.
- Urine chloride differentiates alkalosis: Saline-responsive (vomiting, diuretics) vs Saline-resistant (hyperaldosteronism).
- Diarrhea causes Normal AG Metabolic Acidosis; Vomiting causes Metabolic Alkalosis.
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