Renal Physiology – Acid-Base and Diuretics Study Notes (Part 5)

1. Definitions

• Acidosis: A primary physiologic process causing acidemia (low pH)

  • Respiratory acidosis: Elevated pCO2 due to hypoventilation → ↑ hydrogen ions → ↓ pH

  • Metabolic acidosis: ↑ hydrogen ions or ↓ bicarbonate → ↓ pH

• Alkalosis: A primary physiologic process causing alkalemia (high pH)

  • Respiratory alkalosis: ↓ pCO2 due to hyperventilation → ↓ hydrogen ions → ↑ pH

  • Metabolic alkalosis: ↑ bicarbonate or ↓ hydrogen ions → ↑ pH

2. Respiratory Acidosis

Causes:

• CNS damage affecting breathing centers

• Respiratory tract obstruction

• Decreased gas exchange (e.g., COPD, pneumonia)

Compensation:

• Acute: pH ↓ 0.07 per 10 mmHg ↑ pCO2, HCO3⁻ ↑ ~1 mEq/L per 10 mmHg pCO2

• Chronic: pH ↓ 0.03, HCO3⁻ ↑ 3–4 mEq/L per 10 mmHg pCO2

• Renal compensation takes ~4 days, never fully normalizes pH

• Red flag: HCO3⁻ > 30 mEq/L → possible second process (e.g., metabolic alkalosis)

3. Metabolic Acidosis

Causes:

• Increased anion gap: Formation of excess acid (DKA, lactic acidosis, uremia, aspirin, methanol)

• Normal anion gap (hyperchloremic): Loss of bicarbonate (diarrhea, RTA, renal failure)

Compensation:

• Respiratory: ↑ ventilation → ↓ pCO2

• Takes 12–24 hours

• Winter’s formula: Expected pCO2 = 1.5 × [HCO3⁻] + 8 ± 2

• Approximation: Expected pCO2 ≈ last two digits of pH ± 2

• Deviation:

  • pCO2 lower than expected → concomitant respiratory alkalosis

  • pCO2 higher than expected → concomitant respiratory acidosis

4. Respiratory Alkalosis

Causes:

• Hyperventilation: altitude, drugs, pregnancy, cirrhosis, sepsis

Compensation:

• Acute: pH ↑ 0.08 per 10 mmHg ↓ pCO2, HCO3⁻ ↓ ~2 mEq/L

• Chronic: pH ↑ 0.03, HCO3⁻ ↓ ~5 mEq/L per 10 mmHg pCO2

• Renal compensation can fully normalize pH

Red flag: HCO3⁻ ↓ > 2–4 mEq/L → possible superimposed metabolic acidosis

5. Metabolic Alkalosis

Causes:

• Retention of bicarbonate or loss of hydrogen ions

  • Vomiting, gastric suctioning

  • Diuretics → increased Na⁺ reabsorption → H⁺ secretion

  • Excess corticosteroids or aldosterone

  • Ingestion of alkaline substances

Compensation:

• Hypoventilation → ↑ pCO2

• Approximate: ↑ pCO2 ~5 mmHg per 10 mEq/L HCO3⁻

• Rarely exceeds pCO2 > 50 mmHg unless concomitant respiratory acidosis

6. Anion Gap

• Equation: Na⁺ – (Cl⁻ + HCO3⁻) = 12 ± 4 (8–16)

• Unmeasured anions: albumin, phosphate, sulfate, lactate, keto acids, Ca²⁺, Mg²⁺, K⁺

• Albumin effect: ↓1 g/dL → anion gap ↓ 2.5

• High pH effect: albumin more negative → ↑ anion gap

Mnemonics for high anion gap metabolic acidosis:

• MULE-PACK: Methanol, Uremia, Lactic acidosis, Ethylene glycol, Propylene glycol, Aspirin, Ketoacidosis

• MUD-PILES: Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates

Non-anion gap metabolic acidosis:

• Hyperchloremic acidosis → diarrhea, RTA, carbonic anhydrase inhibitors, Addison’s disease

Delta Delta (ΔΔ):

• Ratio of Δ anion gap / Δ bicarbonate

• ΔΔ < 1 → mixed metabolic acidosis (non-anion gap)

• ΔΔ > 2 → metabolic alkalosis or bicarbonate retention

7. Base Excess

• Represents excess or deficit of base (mainly bicarbonate)

• Normal: –2 to +2 mEq/L

• Negative → metabolic acidosis

• Positive → metabolic alkalosis

8. Approach to Acid-Base Disorders

1. Assess clinical picture

2. Measure pH, pCO2, HCO3⁻

3. Identify primary disturbance:

   • pH ↓ & pCO2 ↑ → respiratory acidosis

   • pH ↓ & HCO3⁻ ↓ → metabolic acidosis

   • pH ↑ & pCO2 ↓ → respiratory alkalosis

   • pH ↑ & HCO3⁻ ↑ → metabolic alkalosis

4. Determine acute vs chronic (respiratory)

5. Check anion gap (metabolic acidosis)

6. Assess expected compensation

7. Identify mixed disorders if compensation deviates

Note: Normal pH does not always mean normal acid-base status

9. Expected Compensation Summary (Simplified)

Respiratory Acidosis:

• Acute: ΔHCO3⁻ ≈ +1 mEq/L per 10 mmHg ↑ pCO2

• Chronic: ΔHCO3⁻ ≈ +4 mEq/L per 10 mmHg ↑ pCO2

Respiratory Alkalosis:

• Acute: ΔHCO3⁻ ≈ –2 mEq/L per 10 mmHg ↓ pCO2

• Chronic: ΔHCO3⁻ ≈ –5 mEq/L per 10 mmHg ↓ pCO2

Metabolic Acidosis:

• Expected pCO2 ≈ 1.5 × [HCO3⁻] + 8 ± 2 or last two digits of pH

Metabolic Alkalosis:

• Expected pCO2 ≈ 0.7 × [HCO3⁻] + 20 ± 5

10. Examples

• Acute respiratory acidosis: OR patient hypoventilating → pH ↓, pCO2 ↑, HCO3⁻ slightly ↑

• Chronic respiratory acidosis: COPD patient → pH mildly ↓, pCO2 ↑, HCO3⁻ significantly ↑ (renal compensation)

• Mixed disorders: Cardiac arrest + lactic acidosis → combined respiratory and metabolic acidosis

11. Diuretics Overview

• Increase urine output → ↓ renal sodium absorption → water follows → increased excretion

• Often cause potassium, chloride, magnesium, calcium loss

• Potassium-sparing diuretics: aldosterone antagonists, sodium channel blockers

• Goal: reduce extracellular fluid volume in edema or hypertension

• Effect over time: increased sodium excretion → gradual reduction in extracellular fluid volume

These notes summarize the main points for renal acid-base physiology and diuretic therapy. They are structured for quick review and exam prep.