Acid-Base Disorders

ABG Basics - pHundamental Facts

• pH: Logarithmic measure of H+; normal range critical for cellular function.
• Regulated by:
  • Chemical buffers (bicarbonate, phosphate, proteins) - immediate action.
  • Lungs: Control PaCO2 (volatile acid via carbonic anhydrase) - rapid response (minutes to hours).
  • Kidneys: Control HCO3- reabsorption/generation & H+ excretion (fixed acids) - slow but potent response (hours to days).
• Key Relationship: $pH \propto \frac{[HCO_3^-]}{PCO_2}$ (Henderson-Hasselbalch principle).
• Compensation: Physiological response to primary acid-base disturbance, aiming to normalize pH.

⭐ Normal arterial blood pH is 7.35-7.45; PaCO2 is 35-45 mmHg; HCO3- is 22-26 mEq/L.

Metabolic Acidosis - Anion Gap Assault

• Anion Gap (AG): Calculated as $Na^+ - (Cl^- + HCO_3^-)$. Normal range: 8-12 mEq/L. Reflects unmeasured anions.
• Respiratory compensation:

  ⭐ For metabolic acidosis, expected PaCO2 (Winter's formula) is $PaCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2$. This assesses respiratory compensation.

• HAGMA (AG > 12 mEq/L): Due to ↑ unmeasured anions.
  • 📌 GOLDMARK:
    • Glycols (ethylene, propylene)
    • Oxoproline (paracetamol)
    • L-Lactate (lactic acidosis)
    • D-Lactate
    • Methanol
    • Aspirin (salicylates)
    • Renal failure (uremia)
    • Ketoacidosis (DKA, alcoholic)
• NAGMA (AG 8-12 mEq/L): Hyperchloremic; $HCO_3^-$ loss or $Cl^-$ gain.
  • 📌 HARDUPS:
    • Hyperalimentation, Hyperchloremia
    • Acetazolamide, Addison's
    • Renal Tubular Acidosis (RTA)
    • Diarrhea (GI $HCO_3^-$ loss)
    • Uretero-sigmoidostomy
    • Pancreatic fistula
    • Saline (excessive IV)

Metabolic Alkalosis - Base Boost Bummers

• Primary disturbance: ↑ $HCO_3^-$, leading to ↑ pH (alkalemia).
• Respiratory compensation: Hypoventilation → ↑ PaCO₂.
  • Expected PaCO₂ ≈ 0.7 * ($HCO_3^-$) + 20 mmHg (±5).
• Key diagnostic: Urine Chloride (UCl⁻).
  • Saline-Responsive: UCl⁻ < 15-20 mEq/L (vomiting, diuretics).
  • Saline-Unresponsive: UCl⁻ > 20 mEq/L (mineralocorticoid excess).

⭐ Saline-responsive metabolic alkalosis (e.g., due to vomiting or prior diuretic use) typically presents with a urine chloride < 15 mEq/L.

Respiratory Disorders - Lung pH Limbo

• Respiratory Acidosis: ↓Alveolar ventilation → ↑$P_{a}CO_2$, ↓pH.
  • Acute Compensation: For each 10 mmHg ↑$P_{a}CO_2$, $HCO_3^-$ ↑ by 1 mEq/L.

  ⭐ In chronic respiratory acidosis, for every 10 mmHg rise in PaCO2 above 40 mmHg, serum HCO3- increases by approximately 3.5-4 mEq/L (up to a maximum of ~35-40 mEq/L).

• Respiratory Alkalosis: ↑Alveolar ventilation → ↓$P_{a}CO_2$, ↑pH.
  • Acute Compensation: For each 10 mmHg ↓$P_{a}CO_2$, $HCO_3^-$ ↓ by 2 mEq/L.
  • Chronic Compensation: For each 10 mmHg ↓$P_{a}CO_2$, $HCO_3^-$ ↓ by 4-5 mEq/L.

ABG Interpretation - ABG Detective Work

Systematic steps:

• 1. pH: Acidemia (<7.35), Alkalemia (>7.45), Normal (7.35-7.45)?
• 2. Primary: PaCO2 (35-45 mmHg) or HCO3- (22-26 mEq/L) match pH?
• 3. Compensate: Expected? (Winter's: $PCO_2 = 1.5 \times HCO_3^- + 8 \pm 2$).
• 4. AG: If Met. Acidosis. $AG = Na^+ - (Cl^- + HCO_3^-)$. Normal 8-12 mEq/L.
• 5. Mixed?: If compensation off, or normal pH + abnormal PaCO2/HCO3-.

⭐ A normal pH (7.35-7.45) with significantly abnormal PaCO2 and HCO3- strongly indicates either a fully compensated simple disorder or a mixed acid-base disorder.

High‑Yield Points - ⚡ Biggest Takeaways

• Anion Gap (AG) = Na - (Cl + HCO3); normal 8-12 mEq/L. High AG in MUDPILES.
• Winter's formula for metabolic acidosis: Expected PaCO2 = (1.5 * HCO3) + 8 ± 2.
• Metabolic alkalosis: Check urine chloride (<15 mEq/L for saline-responsive, >15 mEq/L for saline-resistant).
• Respiratory acidosis: Caused by hypoventilation (e.g., COPD, opioids); results in ↑PaCO2, ↓pH.
• Respiratory alkalosis: Caused by hyperventilation (e.g., anxiety, PE); results in ↓PaCO2, ↑pH.
• Delta-Delta ratio (ΔAG/ΔHCO3) helps identify mixed disorders; ratio 1-2 suggests pure HAGMA.