Lecture 16- O2 and CO2 exchange

What are the typical resting values for O₂ consumption and CO₂ production?

O₂ consumption ​​(V(O2)) = 250–300 mL/min

CO₂ production (V(CO2)) = 200–250 mL/min

What is the respiratory quotient (RQ) and how is it calculated?

RQ = ratio of CO₂ produced to O₂ consumed - RQ= (V(VO2))/(V(O2))

Typical value = 0.8 at rest (200/250)

How does RQ change with different fuel sources?

RQ = 0.7 → exclusive fat metabolism

RQ = 1.0 → exclusive carbohydrate metabolism

RQ = ~0.8 → mixed diet

What does Fick’s Law of Diffusion describe?

The rate of gas transfer across a membrane: F= (A/T)xD(P1-P2)
Where F=flux (amount flowing), A=surface area, T=thickness, D= diffusion constant (doesnt often change), P1-P2= pressure difference

What factors influence the diffusion constant (D) in Fick’s Law?

Diffusion constant depends on gas solubility (S) and molecular weight (MW), as described by Graham’s Law

Why does CO₂ diffuse faster than O₂ across the alveolar membrane?

CO₂ is ~20 times more soluble than O₂ in biological tissues, allowing it to diffuse faster despite its larger molecular weight

How does emphysema affect gas exchange, and which Fick’s Law variable is altered?

Emphysema destroys alveolar walls, dilates spaces, and reduces surface area (A) → decreased diffusion capacity → lower PaO₂

How do pulmonary fibrosis and pulmonary edema impair diffusion, and which Fick’s Law variable is altered?

Both conditions increase thickness (T) of the diffusion barrier:

• Fibrosis: fibrotic tissue thickens alveolar membranes.

• Edema: fluid in alveoli increases diffusion distance.
  Result → reduced diffusion capacity and lower PaO₂.

What is the main driving factor of Fick’s Law in gas exchange?

The pressure gradient (P₁ – P₂) between alveolar gas and arterial blood

How do pressure gradients drive O₂ and CO₂ exchange?

• O₂ diffuses from alveolar PO₂ (PᴀO₂) → arterial PaO₂.

• CO₂ diffuses from arterial PaCO₂ → alveolar PCO₂.

Compare how emphysema, pulmonary fibrosis, and pulmonary edema affect Fick’s Law variables.

• Emphysema → ↓ surface area (A).

• Fibrosis → ↑ thickness (T).

• Edema → ↑ thickness (T).
  All → ↓ diffusion capacity → ↓ PaO₂.

What is the normal alveolar partial pressure of O₂ (PAO₂), and why is it lower than atmospheric PO₂?

PAO₂ ≈ 100 mmHg (vs atmospheric PO₂ 159 mmHg) because air is humidified by water vapour in the alveoli

What three factors determine alveolar PAO₂?

(1) Inspired oxygen pressure (PIO₂), (2) Alveolar ventilation (V̇A), (3) Oxygen consumption (VO₂)

Which factor is most important for controlling PAO₂?

The balance between alveolar ventilation and oxygen consumption (since atmospheric PO₂ is constant)

What is the normal alveolar partial pressure of CO₂ (PACO₂)?

PACO₂ ≈ 40 mmHg

What factors determine PACO₂, and which are most relevant?

Depends on (1) alveolar ventilation, (2) CO₂ production (VCO₂), (3) inspired PICO₂. Since atmospheric CO₂ is negligible, PACO₂ is determined mainly by ventilation vs CO₂ production

How does O₂ diffuse across the alveolar-capillary membrane?

From alveoli (PAO₂ ~100 mmHg) → capillary blood (PaO₂ lower) down its partial pressure gradient

How does CO₂ diffuse across the alveolar-capillary membrane?

From venous blood (PaCO₂ ~46 mmHg) → alveoli (PACO₂ ~40 mmHg) down its partial pressure gradient

What factors affect the rate of alveolar gas diffusion according to Fick’s Law?

1) Alveolar surface area, (2) Thickness of alveolar membrane, (3) Partial pressure gradients (P1–P2, the most important factor)

What are the five main mechanisms of arterial hypoxemia?

(1) Reduced PB or FIO₂, (2) Hypoventilation, (3) Impaired diffusion, (4) Shunt, (5) Ventilation-perfusion (V/Q) mismatch

How does reduced barometric pressure cause hypoxemia?

At high altitude, PB decreases → PIO₂ = FIO₂ × (PB – 47) falls (e.g., Everest: PIO₂ ≈ 43 mmHg) → reduced alveolar PAO₂ and PaO₂

What is hypoventilation and what are its causes?

Decreased alveolar ventilation → lower PAO₂ and less CO₂ removal. Causes: sleep, opioids/barbiturates, chest wall or muscle damage, airway resistance

What is the difference between hypoventilation and hyperventilation?

Hypoventilation decreases PAO₂ and increases PaCO₂; hyperventilation increases PAO₂ and decreases PaCO₂

How do pulmonary fibrosis and emphysema impair diffusion?

Fibrosis increases alveolar membrane thickness; emphysema reduces alveolar surface area → both decrease O₂ transfer into capillaries

What is the normal ventilation-perfusion (V/Q) ratio in the lung, and why?

Normal V/Q ≈ 0.8 (ventilation ≈ 4 L/min; perfusion ≈ 5 L/min) → allows efficient gas exchange and equilibration of O₂/CO₂

What is an anatomical shunt and what does it cause?

Blood bypasses ventilated alveoli (e.g., ventricular septal defect) → no gas equilibration → hypoxemia

What is a physiological shunt?

Alveoli are perfused but not ventilated (e.g., tumor, atelectasis) → blood passes unoxygenated, lowering PaO₂ despite neighboring alveoli compensating

How do low V/Q and high V/Q mismatches differ?

Low V/Q (e.g., emphysema, asthma, edema): ventilation impaired relative to perfusion. High V/Q (e.g., pulmonary hypertension, heart failure): perfusion impaired relative to ventilation. Both reduce gas exchange efficiency.

How does exercise affect gas diffusion according to Fick’s law?

VO₂ increases → larger ΔP (PAO₂ – PaO₂). Alveolar ventilation rises, PAO₂ maintained, more capillaries recruited → ↑ surface area, ↓ diffusion distance → ↑ diffusion capacity