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PY6.1-13 | Respiratory Physiology — Part 2

Lung Volumes and Capacities — Spirometry (PY6.4)

Lung volumes are measured using a spirometer. Understanding these numbers is essential for interpreting pulmonary function tests.

Figure: Lung Volumes and Capacities — Spirometry (PY6.4)

Four primary volumes (non-overlapping):
• Tidal Volume (TV) = volume breathed in or out in a normal breath = 500 mL
• Inspiratory Reserve Volume (IRV) = extra volume you CAN inhale after a normal inspiration = 3,000 mL
• Expiratory Reserve Volume (ERV) = extra volume you CAN exhale after a normal expiration = 1,100 mL
• Residual Volume (RV) = volume remaining in the lungs after maximal expiration = 1,200 mL (CANNOT be measured by spirometry — needs helium dilution or body plethysmography)

Four capacities (combinations of volumes):
• Inspiratory Capacity (IC) = TV + IRV = 3,500 mL
• Functional Residual Capacity (FRC) = ERV + RV = 2,300 mL (the volume at rest, when breathing muscles are relaxed — the equilibrium point between lung recoil inward and chest wall recoil outward)
• Vital Capacity (VC) = IRV + TV + ERV = 4,600 mL (the maximum volume you can move in one breath)
• Total Lung Capacity (TLC) = VC + RV = 5,800 mL

Clinical spirometry patterns:
• Obstructive disease (asthma, COPD): air is trapped → RV increases, FRC increases, TLC increases or normal. FEV₁/FVC ratio < 0.7.
• Restrictive disease (fibrosis, kyphoscoliosis): lung can't expand → all volumes decrease. FEV₁/FVC ratio normal or increased.

Key test: FEV₁ = volume exhaled in the first second of a forced expiration. FVC = total volume exhaled forcefully. Normal FEV₁/FVC = 0.8 (80%). In obstruction, the ratio drops because air can't get out fast enough.

Dead Space — Where Gas Exchange Doesn't Happen (PY6.5)

Not all the air you breathe reaches the alveoli for gas exchange. The volume of air that doesn't participate in gas exchange is called dead space.

Anatomical dead space = volume of the conducting airways (nose to terminal bronchioles) = ~150 mL. Air in this zone never reaches the alveoli.

Alveolar dead space = volume of air that reaches alveoli that are ventilated but not perfused (ventilation without blood flow — gas exchange can't occur). In a healthy person, this is negligible (~negligible mL).

Physiological dead space = anatomical + alveolar dead space. In a healthy person, physiological ≈ anatomical (~150 mL). In disease (e.g., pulmonary embolism blocking blood flow to ventilated alveoli), alveolar dead space increases dramatically.

Bohr equation (calculates physiological dead space):

VD/VT = (PaCO₂ – PECO₂) / PaCO₂

Where VD = dead space volume, VT = tidal volume, PaCO₂ = arterial CO₂, PECO₂ = mixed expired CO₂.

Why this matters:
• Of your 500 mL tidal volume, only 350 mL reaches the alveoli (the rest fills the dead space)
• Alveolar ventilation = (TV – dead space) × respiratory rate = (500 – 150) × 12 = 4,200 mL/min
• Rapid, shallow breathing is inefficient: if TV = 250 mL and RR = 24, minute ventilation = 6,000 mL/min BUT alveolar ventilation = (250 – 150) × 24 = only 2,400 mL/min — dangerously low
• Slow, deep breathing is more efficient: if TV = 1,000 mL and RR = 6, minute ventilation = 6,000 mL/min AND alveolar ventilation = (1,000 – 150) × 6 = 5,100 mL/min

Clinical pearl: This is why patients with rapid shallow breathing (tachypnoea) desaturate despite a normal minute ventilation — most of each tiny breath just washes back and forth in the dead space.

Alveolar Air Composition & Gas Exchange (PY6.6, PY6.7)

Alveolar air is NOT the same as atmospheric air. Here's why:

Gas	Atmospheric air	Alveolar air	Reason
O₂	159 mmHg (21%)	100 mmHg (13.6%)	O₂ is continuously absorbed into blood
CO₂	0.3 mmHg (0.04%)	40 mmHg (5.3%)	CO₂ is continuously delivered from blood
H₂O	Variable	47 mmHg (6.2%)	Air is fully humidified at body temp
N₂	597 mmHg (78.6%)	573 mmHg (75.4%)	Diluted by CO₂ and H₂O

Why is alveolar PO₂ only 100 mmHg, not 159? Because (1) air is diluted with water vapour, (2) CO₂ is added from blood, and (3) O₂ is continuously being absorbed. The alveolar gas equation calculates this:

PAO₂ = PIO₂ – (PACO₂ / R)

Where PIO₂ = inspired PO₂ (corrected for water vapour = 150 mmHg), PACO₂ = alveolar CO₂ (~40 mmHg), R = respiratory exchange ratio (normally 0.8). So: PAO₂ = 150 – (40/0.8) = 150 – 50 = 100 mmHg.

Gas exchange across the respiratory membrane follows Fick's Law of Diffusion:

Rate of diffusion ∝ (Area × Solubility × ΔP) / (Thickness × √MW)

Factors that INCREASE diffusion:
• Large surface area (70 m²) — reduced in emphysema (destroyed alveoli)
• High solubility — CO₂ is 20× more soluble than O₂, so it diffuses much faster despite a smaller pressure gradient
• Large pressure gradient — O₂: 100 (alveolar) → 40 (venous blood) = ΔP = 60 mmHg; CO₂: 46 (venous) → 40 (alveolar) = ΔP = 6 mmHg
• Thin membrane (0.2–0.5 μm) — thickened in fibrosis, oedema

Factors that DECREASE diffusion:
• Thickened membrane (pulmonary fibrosis, oedema)
• Reduced area (emphysema, pneumonectomy)
• Reduced pressure gradient (high altitude — low PIO₂)

Diffusion capacity (DLCO) is measured clinically using carbon monoxide (CO has very high Hb affinity, so its transfer is purely diffusion-limited). Low DLCO = impaired gas exchange membrane.