Applied Respiratory Physiology — Hypoxaemia Acid–Base

Hypoxaemia:

= Hypoxic Hypoxia= decreased PaO2 due to problems at the level of the lungs

Causes:

• Normal A-a Gradient
  • Alveolar hypoventilation – neuromuscular disease
  • Low PiO2 – FiO2 < 0.21, Barometric pressure < 760mmHg
• Raised A-a Gradient
  • Diffusion defect – COPD, Pulmonary fibrosis, exercise
  • V/Q Mismatch – Aging
  • Right-to-left shunt – PDA, PFOs, ASDs or VSDs
  • Increased O2 extraction – Sepsis

Physiological Outcome:

1. ↑ local vasodilation → ↓ SVR and ↓ BP
2. ↓ BP → Baroreceptors → SNS activation → ↑ HR and ↑ C.O.
3. PaO2 < 50-60 mmHg
   • → peripheral chemoreceptors stimulation
   • → ↑ventilation
4. Severe hypoxaemia
   • ↓ HR and BP → shock
   • ↑ CBF (regardless of PaCO2)
5. Lactic Acidosis:
   • Embden-meirhoff continues (glycolysis is anaerobic)
   • Mitochondrial hypoxaemia → ↓d ETC (electron transport chain) activity → ↑ cytoplasmic Acetyl CoA → ↓ conversion of Pyruvate to Acetyl CoA → ↑ [Pyruvate] → ↑ shunting of pyruvate to lactate → ↓ SID → Acidosis (↑ [H])

Chemoreceptor Reflex

• Mechanism:
  • ↓’d perfusion → ↑[H]/↓PaO2 → CR stimulation
    • Afferent signal → Sinus nerve (of herring) / Vagus Nerve → Chemosensitive area of medulla
  • Vasomotor area → ↑ peripheral vasoconstriction
  • Respiratory centre → ↑rate and depth of respiration → ↑ venous return
• Result
  • Hypoxia/hypercaponea → ↑ peripheral vasosmotor tone, ↑rate and depth of respiration
    • ↓ PaO2
      • Gradual ↑ MV PaO2 < 500mmHg,
      • Rapid ↑MV PaO2 < 50 mmHg

Acid-Base changes:

• ↑[H] → ↑rate and depth of respiration → Respiratory alkalosis
  • ↑ HCO3 if chronic (> 3 days)
• ↑[lactate] → ↑ Anion gap

CICMWrecks 2016