Respiratory Acidosis and Alkalosis

Resp Acid-Base Intro - The CO2 Seesaw

• $CO_2$, a metabolic byproduct, acts as a volatile acid. Its partial pressure ($PCO_2$) is the respiratory component of acid-base balance.
• The bicarbonate buffer system: $CO_2 + H_2O \rightleftharpoons H_2CO_3 \rightleftharpoons H^+ + HCO_3^-$. Lungs rapidly adjust $CO_2$.
• Normal arterial $PCO_2$: 35-45 mmHg.
  • ↑$PCO_2$ (e.g., hypoventilation) $\rightarrow$ ↑$H_2CO_3$ $\rightarrow$ ↓pH (respiratory acidosis).
  • ↓$PCO_2$ (e.g., hyperventilation) $\rightarrow$ ↓$H_2CO_3$ $\rightarrow$ ↑pH (respiratory alkalosis).
• Henderson-Hasselbalch equation links pH to $PCO_2$ and $HCO_3^-$: $pH = pKa + log([HCO_3^-] / (0.03 \times PCO_2))$.

The lungs can change $PCO_2$ levels within minutes, making them rapid regulators of acid-base balance. ⭐

Respiratory Acidosis - CO2 Traffic Jam

• Definition: ↓pH (< 7.35), primary ↑$PCO_2$ (> 45 mmHg).

• Pathophysiology: $CO_2$ retention from hypoventilation.

• ABG Findings:

  • Acute: ↓pH, ↑$PCO_2$, $HCO_3^-$ normal or slightly ↑.
  • Chronic: ↓pH (or near normal due to compensation), ↑$PCO_2$, significant ↑$HCO_3^-$ (renal).

• Causes (Hypoventilation):

  • 📌 Mnemonic DEPRESS:
    • Drugs (opioids, sedatives)
    • Edema (pulmonary)
    • Pneumonia
    • Respiratory center depression (CNS lesions, trauma)
    • Emboli (severe Pulmonary Embolism)
    • Spasms (severe asthma, bronchospasm)
    • Sac (alveolar) issues (COPD, ARDS, atelectasis)
  • Others: Guillain-Barré Syndrome (GBS), Myasthenia Gravis, chest wall disorders.

• Clinical Features: Headache, anxiety, blurred vision, confusion, drowsiness, asterixis ($CO_2$ narcosis), warm/flushed skin.

• Compensation (Renal: ↑$HCO_3^-$ reabsorption/generation):

  • Acute: For every 10 mmHg ↑$PCO_2$, $HCO_3^-$ ↑ by 1 mEq/L.
  • Chronic: For every 10 mmHg ↑$PCO_2$, $HCO_3^-$ ↑ by 3-4 mEq/L.

⭐ In chronic respiratory acidosis, for every 10 mmHg increase in PCO2 above 40, serum bicarbonate typically increases by 3.5 to 4 mEq/L.

Respiratory Alkalosis - Hyperventilation Havoc

Primary disturbance: ↑pH, ↓$PCO_2$ (< 35 mmHg) due to $CO_2$ washout from hyperventilation.

• Pathophysiology: Alveolar hyperventilation → ↓Pa$CO_2$ → ↑pH.
• Compensation (Renal): ↓$HCO_3^-$ (↓reabsorption/generation).
  • Acute: $HCO_3^-$ ↓ 2 mEq/L per 10 mmHg ↓$PCO_2$.
  • Chronic: $HCO_3^-$ ↓ 4-5 mEq/L per 10 mmHg ↓$PCO_2$.
• ABG: ↑pH, ↓$PCO_2$, ↓$HCO_3^-$ (compensatory).
• Causes (📌 CHAMPS):
  • CNS disease (stroke)
  • Hypoxia (PE, altitude)
  • Anxiety, pain
  • Mechanical ventilators
  • Progesterone (pregnancy)
  • Salicylates, Sepsis
• Clinical Features:
  • Lightheadedness, paresthesias (circumoral, digital).
  • Tetany, carpopedal spasm (due to ↓ionized $Ca^{2+}$ as ↑pH binds $Ca^{2+}$ to albumin).
  • Seizures (severe).

⭐ Salicylate toxicity classically presents with mixed respiratory alkalosis (direct respiratory center stimulation) and metabolic acidosis.

ABG Clues & Compensation - pH Puzzle Solver

Systematic ABG: 1. pH (Acidemia/Alkalemia) 2. $PCO_2$ (Respiratory) 3. $HCO_3^-$ (Metabolic). Identify primary disorder.

• Resp. Acidosis Comp.:
  • Acute: $HCO_3^-$ ↑ 1 per 10 ↑$PCO_2$.
  • Chronic: $HCO_3^-$ ↑ 3-4 per 10 ↑$PCO_2$.
• Resp. Alkalosis Comp.:
  • Acute: $HCO_3^-$ ↓ 2 per 10 ↓$PCO_2$.
  • Chronic: $HCO_3^-$ ↓ 4-5 per 10 ↓$PCO_2$.
• Mixed disorders: Multiple primary issues.

⭐ If measured compensation differs significantly from expected, suspect a mixed disorder.

High‑Yield Points - ⚡ Biggest Takeaways

• Respiratory acidosis: ↓pH from hypoventilation causing ↑PCO2; renal HCO3- retention compensates.
• Respiratory alkalosis: ↑pH from hyperventilation causing ↓PCO2; renal HCO3- excretion compensates.
• PCO2 is the primary driver in respiratory acid-base disorders.
• Renal compensation is slow, taking hours to days to adjust HCO3-.
• Acute respiratory acidosis: minimal HCO3- change; Chronic: significant ↑HCO3-.
• Common causes: Acidosis - COPD, sedatives; Alkalosis - anxiety, hypoxia, PE.