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Metabolic Acidosis and Alkalosis

Metabolic Acidosis and Alkalosis

Metabolic Acidosis and Alkalosis

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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:
  • Anion Gap (AG) = $Na^+ - (Cl^- + HCO_3^-)$. Normal AG: 8-12 mEq/L.

  • Types & Causes:

    CategoryMnemonicKey Causes
    High Anion Gap (HAGMA)📌 GOLDMARK / MUDPILESGlycols (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📌 HARDUPHyperalimentation / 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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