Alveolar ventilation and gas exchange

Question 1

B1

Describe oxygen cascade

Answer 1

• atmospheric air
• airway gas
• alveolar gas
• endcapillary blood
• arterial blood
• tissue e.g. brain
• nitochondria
  • humidification: brings partial pressure down, mixes with water vapour, suppressing oxygen content
  • Dilution by CO2
  • venous admixture i.e. through shunts
  • arterial-> tissue: level of CO2
  • ^ tissue to mitochondria

Question 2

Describe the concept of ideal alveolar gas

and caveats

Answer 2

concentration that would exist if
- Equal ventilation and perfusion
- PACO2 = PaCO2 = 40mmHg
- PAO2 = FiO2 x (PB - SVP H2O) – (PaCO2/RQ)
- PAO2 = 0.21 x 713 – (40/0.8)
- PAO2 = 100mmHg
- Non-Uniformity: Ventilation and perfusion not uniform across lung in reality. This gives rise to various gas concentrations across the alveoli, which are worsened by lung pathology

Question 3

Describe effect of changes to VQ matching

Answer 3

decreasing V/Q= poorer ventilation - high PCO2, low PO2
- shunt: areas of lung perfused not ventilated
- increasing V/Q -inverse - high oxygen, low pCO2 ~ atmospheric gas ^[minus svp]
- dead space: areas of lung ventilated not perfused

• V/Q a spectrum across lung and across disease states
  - areas of lung ‘fall along line’
  - lower in lung, lower V/Q “shunt” (more blood here)
  - upper lung, higher V/Q, more ‘dead space’
  - ideal area rib 3: V, Q optimal i.e. ‘middle’ part of lung

Question 4

Define and describe dead space

Answer 4

Dead Space
is the volume of inspired air that does not participate in gas exchange
- Anatomical Dead Space: In conducting airways ^[n.b. get clear definitions for upper lower airways/disease]
- Normal value: ~2.2ml/kg or 150ml in adults
- Factors that vary/increase Dead Space
- Increased size of conducting airways
- Infants
- Neck, jaw position ^[how?]
- Lung volume
- Intubation: Introduces apparatus dead space
- can be measured using Fowler’s

• Alveolar Dead Space: Gas to alveolus without gas exchange, due to inadequate perfusion
  
  • Small value, but increased in conditions like PE, postural hypotension and upper lobes of lungs
• Physiological Dead Space: Sum of anatomical and alveolar dead space
  
  • Measured using Bohr equation ^[concept over formula]
  • VD/VT = PaCO2 – FECO2 / PaCO2
  • Note: **only a small gradient, typically, between PaCO2 and FeCO2 ^[Pa slightly higher]
    
    • but is increased in anything leading to V/Q mismatch (increase)

Question 5

Distinguish between physiological and anatomical dead space

Answer 5

• Alveolar Dead Space: Gas to alveolus without gas exchange, due to inadequate perfusion
  
  • Small value, but increased in conditions like PE, postural hypotension and upper lobes of lungs
• Physiological Dead Space: Sum of anatomical and alveolar dead space
  
  • Measured using Bohr equation ^[concept over formula]
  • VD/VT = PaCO2 – FECO2 / PaCO2
  • Note: **only a small gradient, typically, between PaCO2 and FeCO2 ^[Pa slightly higher]
    
    • but is increased in anything leading to V/Q mismatch (increase)

Question 6

Define and describe shunt

Answer 6

• Shunt: Blood bypasses ventilated lung areas a.k.a does not undergo gas exchange, e.g. passing unventilated alveoli ^[in other words: venous blood enters arterial circulation]
  
  • Venous Admixture: amount Mixed venous blood added to end-capillary blood to produce observed difference between arterial and pulmonary-end capillary blood

Question 7

List some anatomical and pathological causes of shunt

Answer 7

• Anatomical (e.g. thesbian ^[drain heart] and bronchian veins ^[drain lung])
  
  • Pathological: anything that impairs gas getting to, and across, the alveolar membrane (pneumonia, atelectasis…)

Question 8

What is the clinical relevance of shunts

Answer 8

• shunted blood by definition is not exposed to ventilated alveoli
  
  • **Increased concentration O2 in alveoli, therefore, won’t improve O2 in shunted blood
    
    • may slightly increase SaO2 if only a small shunt ^[e.g. oxygenating post-op anaesthetic patient, lung bases collapsed, poorly ventilated–worsens with age, size]
  • > 30% shunt : unlikely to see SaO2 changes ^[need to solve structural issue]
• A-a Gradient: in general, >20mmHg suggests pathological shunt ^[n.b. can’t clinically measure, A-a gives proxy]

Question 9

How is pathological shunt determined in a clinical setting?

Answer 9

• A-a Gradient: in general, >20mmHg suggests pathological shunt ^[n.b. can’t clinically measure, A-a gives proxy]

Question 10

Describe determinants of alveolar gas exchange

Answer 10

• Ideal Alveolus: PAO2 100mmHg, PACO2 40mmHg
• Factors Affecting Gas Movement (O2 to blood, CO2 to alveolus )
  
  • Fick’s Law of Diffusion
    
    • Rate of diffusion = (A/T) x (Sol/ √MW) x (C1 – C2)
    • A = Area, T = Thickness, Sol = Solubility, MW = Molecular weight
  • Area: Large surface area for diffusion. Factors that cause shunt = factors that affect surface area
  • Thickness: Diffusion membrane thin (0.5µm) and comprise type I alveolar cells, basement membrane, and endothelium - thickness typically comes from alveolar side e.g. in p fibrosis
  • Solubility and Molecular Weight: Fixed for gas type. Note CO2 is 20x more soluble than O2
  • Concentration Gradient
    
    • CO2: Mixed venous CO2 46mmHg – Alveolar CO2 40mmHg = 6mmHg gradient
      
      • note: small gradient but still very soluble, still corresponds to 200ml/min of Co2 diffusion
      • CO2 very soluble thus hypercapnoea extremely unlikely due to diffusion issues– but instead due to inadequate ventilation *relative to metabolic demand
    • O2: Mixed venous O2 40mmHg – Alveolar O2 100mmHg = 60mmHg gradient
      
      • much larger O2 gradient
      • accounts for low solubility
      • diffusion = 250 ml/min
      • **diffusion is complex, not purely dependent on pressure gradient, but also:
        
        • O2- Hb reaction to maintain pressure gradient
        • rate of pulmonary blood flow

Question 11

Distinguish between concentration gradient that is perfusion limited or diffusion limited

Answer 11

• Perfusion Limited
  
  • Capillary partial pressure quickly approaches alveolar pressure
  • Concentration gradient depends on delivery of fresh pulmonary end capillary blood a.k.a dependent on blood flow, not gas diffusion capacity
  • E.g., N2O behaves this way, O2 behaves this way under normal conditions
• Diffusion Limited
  
  • Capillary partial pressure approaches alveolar pressure *very slowly
  • Increased perfusion therefore has minimal impact on capillary partial pressure
  • Instead determined by ability of gas to diffuse well
  • CO is an example, high affinity for Hb, so gradient determined by diffusion ability
    - DCCO: CO used to measure diffusion capacity of lungs

Question 12

Describe under what conditions is oxygen perfusion limited or diffusion limited

Answer 12

• Perfusion vs Diffusion for Oxygen
  
  • Normally perfusion limited (0.2-0.3s equilibration with capillary blood)
  • Gas exchange impaired if diffusion membrane affected, to the point where oxygen becomes diffusion limited instead of perfusion limited:
    
    • initially this will only be seen with decreased capillary transit times (e.g. exercise)
    • (can happen at rest with severe conditions)
• ## Clinical Implication: Impaired diffusion membrane affects gas exchange, especially for oxygen