Applied Resp – Gases

Master answer

Therefore, owing to equation (2) and the haemoglobin dissociation curve, at P_aO₂ > 100mmHg there is:

            Only a minimal increase in haemoglobin saturation
            Only a minimal increase in dissolved oxygen concentration

Oxygen stores

Functional residual capacity = lung volume with no active insp. or exp. effort
   = volume when equilibrium between chest wall recoil and lung elastic recoil

If F_iO₂ increased → more oxygen in FRC (not exhaled with tidal volume)
→ Able to tolerate a period of hyperventilation

Absorption atelectasis

• Nitrogen is an inert gas, comprising ~78% of room air
• As it is biologically inert, it is in equilibrium throughout body tissues
  • There is no concentration gradient to cause absorption from the lungs
• If F_iO₂ increased
  • P_iO₂ of O₂ increases
  • P_aN₂ decreases as a result
  • Moves out of alveoli down its concentration gradient
    • ∴Total alveolar pressure falls -> alveolar collapse
• Clinically significant when F_iO₂ > 50%

Hypoxic vasoconstriction

• In under ventilated lungs portions, there is adaptive pulmonary vasoconstriction, reducing V/Q mismatching
• If F_iO₂ increased
  • Under ventilated lung portions have a higher P_aO₂
    • V/Q mismatching -> venous admixture, ↓ pulmonary vein P_AO₂

Haldane effect

Deoxygenated haemoglobin has a higher affinity for CO₂ than oxygenated Hb

If SaO₂ is artificially raised, lower CO₂ carrying capacity -> build-up of CO₂ in tissues

Oxygen radicals

• A radical is a molecule with an unpaired electron outside of an electron shell
  • Highly reactive, cause tissue damage
• Important reactive oxygen species (ROS): Superoxide radical (O₂^–); peroxide radical (O₂^2-); hydroxide radical (•OH)
• ROS can usually be eliminated by cellular antioxidant defence mechanisms
• When F_iO₂ > 50%
  • Defense mechanisms overwhelmed
  • Paranchymal injury
    • Tracheobronchitis
    • Pulmonary capillary endothelial damage -> pulmonary oedema + fibrosis

Mooney 2016

Answer by Mooney